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283 ISBN 978 1 4202 3217 2 Memories are not stored in any one specific brain location. They are stored throughout the brain and linked together through neural pathways, often described as ‘memory circuits’, made up from interconnected neurons. This does not mean that all areas of the brain are equally involved in memory. Different brain areas and structures are active as we encode, store and retrieve different types of information. Specific brain areas are also more or less involved in different memory processes. For example, the temporal lobes have an important role in declarative explicit memories (‘knowing that’), but are less important for procedural implicit memories (‘knowing how’). In this chapter, we examine the neural basis of memory. We start with changes in the brain at the neuronal level when memories form. Role of the neuron in memory formation A neuron is a nerve cell that is specialised to receive, process and/or transmit information to other cells within the body. Neurons communicate with each other, and muscles and glands. Often referred to simply as ‘nerve cells’, neurons are the building blocks and basic working units of the brain and nervous system. Neurons vary in shape and size depending on where they are located and on their specific function. However, most neurons typically have three main structural features: dendrites, a soma and an axon. Dendrites are the thin extensions of a neuron that receive information from other neurons and Mechanism of memory formation 7 transmit it to the soma. As shown in figure 7.1, on the next page, the dendrites separate out like the branches of a tree. Some dendrites have additional little extensions, or ‘outgrowths‘, called dendritic spines. Each spine represents a point a neuron can connect with and receive information from a neighbouring neuron. A single neuron can have thousands of connections to other neurons through its dendritic branches and spines. The soma, or cell body, integrates the neural information received from dendrites and sends it to the axon. It contains the nucleus (which houses the cell’s genetic code), organelles (other structures) and cytoplasm (liquid gel) that maintain the neuron and keep it functioning. In most neurons, the soma is located centrally. The axon is a single, tube-like extension that carries neural information away from the soma towards other neurons (or cells in muscles or glands). Many axons split into smaller branches called axon collaterals. At the end of the collaterals are axon terminals. Each axon terminal has a small knob-like swelling at its tip called a terminal button (sometimes called a synaptic vesicle, synaptic knob or synaptic button). The terminal button is a small structure like a sac that stores and secretes neurotransmitter manufactured by the neuron. Information travels along the axon as an electrical impulse called an action potential (or neural impulse). Myelin, a white fatty substance, coats and insulates the axon—but not all neurons are myelinated. The myelin sheath around the axon serves a similar function as the insulation around electrical wire and helps prevent interference from

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283ISBN 978 1 4202 3217 2

Memories are not stored in any one specific brain location. They are stored throughout the brain and linked together through neural pathways, often described as ‘memory circuits’, made up from interconnected neurons. This does not mean that all areas of the brain are equally involved in memory. Different brain areas and structures are active as we encode, store and retrieve different types of information. Specific brain areas are also more or less involved in different memory processes. For example, the temporal lobes have an important role in declarative explicit memories (‘knowing that’), but are less important for procedural implicit memories (‘knowing how’). In this chapter, we examine the neural basis of memory. We start with changes in the brain at the neuronal level when memories form.

Role of the neuron in memory formationA neuron is a nerve cell that is specialised to receive, process and/or transmit information to other cells within the body. Neurons communicate with each other, and muscles and glands. Often referred to simply as ‘nerve cells’, neurons are the building blocks and basic working units of the brain and nervous system. Neurons vary in shape and size depending on where they are located and on their specific function. However, most neurons typically have three main structural features: dendrites, a soma and an axon.

Dendrites are the thin extensions of a neuron that receive information from other neurons and

Mechanism of memory formation7

transmit it to the soma. As shown in figure 7.1, on the next page, the dendrites separate out like the branches of a tree. Some dendrites have additional little extensions, or ‘outgrowths‘, called dendritic spines. Each spine represents a point a neuron can connect with and receive information from a neighbouring neuron. A single neuron can have thousands of connections to other neurons through its dendritic branches and spines.

The soma, or cell body, integrates the neural information received from dendrites and sends it to the axon. It contains the nucleus (which houses the cell’s genetic code), organelles (other structures) and cytoplasm (liquid gel) that maintain the neuron and keep it functioning. In most neurons, the soma is located centrally.

The axon is a single, tube-like extension that carries neural information away from the soma towards other neurons (or cells in muscles or glands). Many axons split into smaller branches called axon collaterals. At the end of the collaterals are axon terminals. Each axon terminal has a small knob-like swelling at its tip called a terminal button (sometimes called a synaptic vesicle, synaptic knob or synaptic button). The terminal button is a small structure like a sac that stores and secretes neurotransmitter manufactured by the neuron.

Information travels along the axon as an electrical impulse called an action potential (or neural impulse). Myelin, a white fatty substance, coats and insulates the axon—but not all neurons are myelinated. The myelin sheath around the axon serves a similar function as the insulation around electrical wire and helps prevent interference from

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the activity of other nearby axons. The myelin sheath is not a continuous coating, extending the full length of the axon. It occurs in segments that are separated by unmyelinated gaps called nodes of Ranvier. Neurons wrapped in myelin typically communicate their messages much faster than unmyelinated neurons.

Information always travels in one direction through a neuron. It is received by dendrites, passes through the soma and exits from the axon. An action potential originates at the soma. When it reaches the axon terminals, it stimulates the release of neurotransmitter from the terminal buttons. The neurotransmitter carries the message to other neurons. Although each neuron has only one axon, the collaterals and axon terminals allow its message to be sent to many other neurons.

When neurons communicate with one another, they do so by sending neurotransmitter across the tiny space between the terminal buttons of one neuron, which release the neurotransmitter,

Axon

Soma

Dendrite

Figure 7.1 Neurons are nerve cells that transmit information throughout the entire nervous system. They have three main structural features: dendrites for receiving information from other neurons, a soma that integrates this information, and an axon that transmits the information to other neurons. Information generally flows in one direction through the neuron—from dendrites towards the soma and away from the soma along the axon.

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AxonMyelin sheath

Nodes of Ranvier

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Terminal buttons

and the dendrites of another, which receive the neurotransmitter. This tiny space is called the synaptic gap (or synaptic cleft). The synaptic gap is about 500 times thinner than the thinnest strand of your hair. It is one component of the synapse. The other two components of the synapse are the terminal buttons of the presynaptic (‘sending’) neuron and the dendrites of the postsynaptic (‘receiving’) neuron. The synapse is the site where communication occurs between adjacent neurons. It is also believed to be a site for memory storage, but how memories are actually stored is still unclear (Kandel, 2009).

Neurotransmitter is a chemical substance produced by a neuron that carries a message to other neurons or cells in muscles and organs. When carrying a message to another neuron, neurotransmitter works by attaching itself (‘binding’) to receptor sites of postsynaptic neurons that are specialised to receive that specific neurotransmitter. Neurotransmitter that does

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not bind to receptors in the postsynaptic neuron is taken up again by the presynaptic neuron in a process called reuptake. Generally, a specific type of neurotransmitter will have either of two effects. Some neurotransmitters have an excitatory effect and consequently stimulate or activate

postsynaptic neurons. Other neurotransmitters have an inhibitory effect and block or prevent postsynaptic neurons from firing. The process of neurons communicating with one another is called neurotransmission (or synaptic transmission).

Changes in function and structure of neurons Research findings indicate that significant changes occur in the function and structure of brain neurons involved in memory formation. These changes do not occur independently of each other and both are required to process newly learned information for memory and enable long-term storage.

Change in the function of neurons is evident in:

• an increase in the amount of neurotransmitter produced and released by the presynaptic neurons, and/or

• greater effects of neurotransmitter at its receptor sites on the postsynaptic neurons. Different neurotransmitters tend to have

different roles in memory formation. Researchers have yet to entirely isolate or explain the specific effects of each one. Generally, they all enable communication of the information to be encoded and initiate or contribute to important structural changes at the synapse that help ensure the memory is durable (long-lasting) when formed. Four specific types of neurotransmitter implicated in memory formation are glutamate, dopamine, acetylcholine and norepinephrine.

Glutamate (Glu) is the main excitatory neurotransmitter for information transmission throughout the brain. This means that glutamate enhances information transmission by making postsynaptic neurons more likely to fire. In memory formation, glutamate plays crucial roles in the structural changes that occur, particularly in the growth and strengthening of synaptic connections between neurons within a memory circuit. However, specific types of glutamate receptors also have to be present for glutamate to have these effects. Two of these receptors are called NMDA and AMPA. In particular, NMDA (N-methyl-D-aspartate) specialises in receiving glutamate and is found in abundance at the hippocampus, a key structure involved in the formation of LTM.

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Synapse

Terminal buttons

DendritesSoma (cell body)

Axon

Myelin sheath(surrounds andinsulates the axon)

Figure 7.2 Neurons do not link together like a chain. The branches of an axon almost touch the dendrites of the next neuron, leaving a tiny space called a synaptic gap.

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Dendrite of postsynaptic (receiving) neuron

Synaptic gap

Action potential (neural impulse)

Terminal buttons

Axon terminal

NeurotransmitterReceptor sites

Figure 7.3 Within the neuron, the message is called an action potential. When this reaches the axon terminal, neurotransmitter is released from the terminal buttons, travelling across the synaptic gap to the receiving neuron.

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Dopamine (DA) has a number of roles including attention, initiation of voluntary movement, the experience of pleasure and reward-based learning. It has also been found to contribute to the strengthening of synaptic connections in the brain and therefore to the formation of LTM. This role is similar to that of glutamate but does not seem to be as prominent or as well understood. There also seems to be an ideal level of dopamine for working memory to function properly. As the level of dopamine increases or decreases, so can the functioning of working memory.

Acetylcholine (ACh), which is also involved in learning, attention, sleeping, dreaming and motor control, is found to be at an abnormally low level in the brains of people suffering from Alzheimer’s disease, a type of dementia that is characterised by the gradual deterioration of memory, resulting in very serious memory deficits. Furthermore, drugs that inhibit the activity of ACh can cause temporary loss of memory.

Norepinephrine (NE) has a role in the encoding and retention of memories for emotionally significant experiences. Norepinephrine, also called noradrenaline, occurs as both a neurotransmitter and ‘stress hormone’ and is secreted automatically during times of heightened emotional arousal. It affects memory by influencing the activities of the amygdala and hippocampus, two adjacent brain structures with crucial roles in memory formation.

It is believed that level of emotional arousal during the time of encoding influences the strength of the long-term memory of that event. The presence of increased levels of norepinephrine at the amygdala during emotional arousal communicates to the hippocampus that details of the relevant experience are significant and therefore stronger encoding and storage are required. The hippocampus then uses this information to strengthen the storage of the emotional information in declarative memory (Hamann, 2009).

A second type of change that occurs in neurons during memory formation is to their structure. Structural change essentially involves the growth and strengthening of synaptic connections. When a new memory is being formed, the number of dendritic spines increases and the dendrites therefore become ‘bushier’. This has the effect of increasing the surface area of the dendrites, thereby

allowing for extra synapses. Synaptic growth (or ‘extra synapses’) allows for more synaptic connections between adjacent neurons in a memory circuit. These synaptic connections are believed to be the mechanism of memory storage, providing a place for storing memories and allowing us to remember for as long as we do (Kandel, 2009).

The functional and structural changes at the neuronal level create a memory circuit. Within the circuit, synaptic growth strengthens the connections between the neurons in the circuit. Each time the memory is retrieved, the neurons are activated. The functional and structural changes recur and further strengthen the communication links within the circuit and the establishment of the memory in long-term storage.

The synaptic changes that take place within a memory circuit are described as having long-term potentiation. Long-term potentiation (LTP) refers to the long-lasting strengthening of synaptic connections of neurons, resulting in the enhanced or more effective functioning of the neurons whenever they are activated. Basically, the effect of LTP is to improve the ability of two neurons—a presynaptic and a postsynaptic neuron—to communicate with one another at the synapse. LTP strengthens synaptic connections in a way that 07005

Glutamate

ACh

Figure 7.4 Each neurotransmitter has a chemically distinct shape. Like a piece of a jigsaw puzzle, or a key in a lock, a neurotransmitter must perfectly fit the receptor site on the receiving neuron in order to communicate its message.

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enables the postsynaptic neurons to be more easily activated. The postsynaptic neurons become more and more responsive to the presynaptic neurons as a consequence of repeated stimulation. The more you use the information being remembered, the more the LTP process strengthens the memory

circuit, making it easier to retrieve. It is believed that LTP is an essential mechanism of memory formation and that it also makes learning possible (see box 10.2 in chapter 10). But precisely how LTP leads to the formation of long-term memories remains unclear.

Box 7.1Within-neuron transmission of information—the action potentialAn action potential (or neural impulse) is a brief electrical impulse that carries neural information along an axon. It originates in the soma and usually develops as a result of the neuron being stimulated by neurotransmitter.

Action potentials do not travel continuously along the axon. When an action potential is triggered, one section of the axon opens up, which then triggers the next section to open up and so on, passing the impulse along the axon. This is similar to the movement of a coordinated ‘Mexican wave’ through a big crowd of people.

Neurons are surrounded by a membrane (‘casing’). Between the neuron and the membrane is a small amount of fluid that contains particles called ions. Ions are either positively charged or negatively charged. There are different quantities of positively and negatively charged ions within a neuron and in the fluid that surrounds each neuron. This

difference in the charges between the neuron and the surrounding fluid results in an electrical charge across the cell membrane. When the neuron is in its resting state (i.e. when it is not involved in transmitting an action potential), there is a very small difference in the electrical charge inside and outside the neuron. The difference in the electrical charge inside and outside the neuron is called its resting potential.

Each neuron requires a minimum level of stimulation in order to be activated from its resting potential and therefore for an action potential to begin. This minimum level of stimulation required to activate a neuron is called the neuron’s threshold. When messages arrive from other neurons, the resting potential (electrical charge) of a neuron changes. If the electrical charge reaches the threshold, an action potential is activated and begins its movement along the axon (figure 7.5). This movement

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Som

aS

oma

Neural impulse Axon

Action potential

Action potential

Som

a

Figure 7.5 Inside the axon is usually negatively charged, while the fluid that surrounds the axon is usually positively charged. As an action potential travels along the axon, these charges reverse. Inside the axon becomes positively charged while the surrounding fluid becomes negatively charged.

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occurs in sections. At the end of each section of the axon are ion channels. The ion channels are like gates that open and close to allow ions to flow along the axon. As the impulse moves down the first section of the axon from the soma, the ‘gate’ opens, enabling the impulse to move into the second section. The gate then closes after the impulse has passed into the next section. The closure of the gate after the impulse has moved onto the next section of the axon prevents the impulse from reversing its direction. Thus, the impulse can only move in one direction—from the soma, along the axon to the axon terminals.

Once an action potential has been triggered, it is self-sustaining. It will continue to the end of the axon without further stimulation. As long as the neuron is stimulated to its threshold, an action potential will occur. Regardless of the amount of stimulation above the threshold, the

same response will occur. There is no difference in the intensity of an action potential. There is either an action potential or there is no action potential—a neuron either ‘fires’ or does not fire. There is no such thing as a partial action potential. This is called the all-or-none principle.

The speed at which an action potential travels down the axon varies. The fastest can travel around 430 kilometres per hour. The slowest travel at around 3.5 kilometres per hour. The speed of transmission depends mainly on two factors: the diameter (width) of the axon and whether the axon has a myelin sheath. The larger the diameter of the axon, the faster the impulse is transmitted. In addition, most of the axons with larger diameters are myelinated and this covering enables the axons to transmit the impulse at a faster speed.

Learning Activity 7.1 Review questions1 Draw a diagram of a neuron and label key

structural features.2 What is the difference between a synapse and

synaptic gap?3 What is synaptic growth?4 What is a ‘memory circuit’?5 Describe the role each of the following has in

memory formation:

a the axon and its terminalsb dendritesc synapsesd synaptic connectionse neurotransmitters.

6 Explain the mechanism of memory formation with reference to functional and structural changes at the neuronal level.

Learning Activity 7.2 Diagram of the role of the neuron in memoryDraw a diagram to summarise the role of the neuron in memory formation. Your diagram should:• include at least two adjacent neurons,

with labels for key structures, areas and substances, as well as brief descriptions of their functions in memory formation

• refer to the role of axons, dendrites, synapses and specific neurotransmitters

• briefly explain the role of the neuron in memory formation.

Use point-form for all descriptions and explanations.

Learning Activity 7.3Role-play on the role of the neuron in memoryWorking in a group of four or five, prepare a role-play that demonstrates and explains the formation of a new ‘memory circuit’ with reference

to dendrites, axons, synapses and specific neurotransmitters.

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Role of the temporal lobe—hippocampus and amygdala In 1957, the publication of a case study drew the attention of psychologists throughout the world to the importance of the temporal lobe in memory. The case study documented memory problems experienced by American patient H.M. The patient, whose real name was Henry Molaison, subsequently participated in hundreds of research studies on memory until he died in 2008 at age 82. However, until his death, he was known only by the initials H.M. to protect his privacy.

In 1953, when Molaison was 27 years old, he agreed to brain surgery to treat the severe epilepsy from which he had been suffering since the age of ten. As with patients who undergo split-brain surgery, Molaison’s epilepsy was unresponsive to anti-convulsant medications and other treatments. It was also extremely debilitating and he had difficulty holding even a simple job. At the time, doctors knew that, in many patients with epilepsy, seizures started in either the right or left hemisphere, usually in the medial temporal lobe.

The medial temporal lobe is the inner surface area at the base of and towards the middle (‘medial’) of the temporal lobe. This area includes the hippocampus; the amygdala, which is next to and touches the hippocampus; and other cortical tissue. Because Molaison’s seizures were so severe, and because their precise origin could not be determined, his neurosurgeon decided to remove the medial temporal lobe from each hemisphere. Altogether, about 5 centimetres of tissue was ‘sucked out’ from each lobe. This included about two-thirds of each hippocampus, most of each amygdala, and cortex from around the hippocampus and amygdala. Although some of the hippocampus and amygdala remained in each lobe, these structures and surrounding neural tissue were so damaged that what was left was useless (Milner & Corkin, 2010).

Medically, the surgery was successful. Molaison’s seizures declined in their frequency and severity, and could also be controlled with medication. His personality was basically unchanged and almost all cognitive functions remained unaffected. Molaison could conduct a conversation as normally as most people do,

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Frontal lobes

Temporal lobes

Medial temporal lobes

Areas removed

Figure 7.6 (a) and (b) Location of the hippocampus and amygdala in the medial temporal lobe area. Henry Molaison had the hippocampus, amygdala and surrounding cortex in the medial temporal lobe area of each hemisphere surgically removed to treat his epileptic seizures. As a result, he lost certain past episodic memories and was incapable of forming new long-term declarative memories—both episodic and semantic memories.

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Temporal lobe

Amygdala

Amygdala

Hippocampus Hippocampus

(a)

(b)

as long as he was not distracted. He had a good vocabulary, normal language skills and slightly above-average intelligence. However, there was a huge cost. The surgery left him with serious memory problems.

Molaison could not remember things that happened in the period leading up to his operation. This memory loss was more or less ‘total’ for about 2 years pre-surgery and ‘partial’ back to about

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10 years pre-surgery. Overall, in relation to episodic memories, he could not remember any event that happened at a specific time and place but he had retained the gist of personal experiences. He could describe in a general way his life up until his operation. He could talk about experiences, but could not report specific details. More significantly, Molaison was incapable of forming new long-term episodic memories or semantic memories (which together constitute declarative memory). For example, Molaison could no longer remember what he had eaten for breakfast when asked shortly afterward, or why he was in hospital. He had to be reintroduced to his doctors every time he visited them, including Brenda Milner, his neuropsychologist who tested him regularly for some 50 years. Molaison had almost no knowledge of current events because he forgot the news almost as soon as he had seen or heard something. He had no idea of what time of day it was unless he had just looked at a clock, and each time he was told his uncle died he reacted with surprise but could never actually experience sadness.

Molaison’s short-term working memory was relatively normal. For example, he could amuse himself doing crossword puzzles. And, if given a series of numbers to learn during psychological testing, he could recall about seven numbers like most people. As long as he paid attention to a task and thought about or actively rehearsed it, he could retain information in short-term memory (and therefore conscious awareness) for as long as required. However, as soon as he was distracted and his attention was therefore diverted to something else, he immediately forgot about it. The information vanished without a trace and could not be recalled thereafter (Ogden & Corkin, 1991).

Molaison could also learn and retain new skills, so formation of new long-term procedural memories was relatively normal. For example, he learnt a new motor skill involving ‘mirror drawing’ for which he had to trace around a shape such as a star that could only be seen in a mirror. He progressively improved with practice on this and other motor learning tasks over a period of days. However, he could never recall having seen the test materials on previous occasions.

Molaison’s case and findings of other research studies provide evidence that the temporal lobe,

specifically the medial temporal lobe area and its key structures, have crucial roles in long-term memory. We consider the specific roles of the hippocampus and amygdala.

Role of the hippocampusJust above each ear and about 4 centimetres straight into the brain is the hippocampus. The hippocampus is a medial temporal lobe structure that is crucial for long-term memory formation (but not all LTM types). LTP, an important mechanism of memory, was first discovered in the hippocampus of rabbits. As shown in figures 7.6 and 7.7, the hippocampus is tubular and curved, somewhat like the shape of a seahorse (after which it is named). In humans, it is about 3.5 centimetres long and we have two of them—one in each hemisphere.

The hippocampus has a crucial role in forming or encoding new declarative explicit memories (semantic and episodic) but not directly in forming or retrieving implicit procedural memories. This role is sometimes referred to as consolidation, a process that involves strengthening of newly forming memories to enable their permanent storage.

Damage to the hippocampus does not seem to seriously affect storage or retrieval of procedural memories, but formation and retrieval of declarative memories are affected. Given that damage does not affect short-term storage or working memory in any significant way, this provides evidence that STM (or working memory) is different from LTM and that the hippocampus is not involved in short-term storage. It is believed that the hippocampus does not store long-term memories. Instead, the hippocampus transfers memories to other cortical areas for long-term storage. The storage most likely occurs in areas involved in processing that type of information.

Although surgery to remove both medial temporal lobes is no longer performed as a treatment for epilepsy, case studies of patients with injury or disease to the hippocampus or hippocampal area in both lobes indicate that they experience the same type of amnesia (called anterograde amnesia) and difficulties forming new long-term explicit memories, although not as severe. Removal of the hippocampus in the

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temporal lobes of other mammals such as rats, rabbits and monkeys results in the same types of memory problems (Zola-Morgan & Squire, 1993; Gluck, Mercado & Myers, 2008).

Why is it that removal of hippocampal areas resulted in Molaison being unable to form new explicit memories for facts and experiences but being able to remember old ones? The hippocampus is widely described as our ‘memory formation area’, the place where our brain temporarily holds and processes components of the information to be remembered. For example, an episodic memory of a rock concert you attend will have different components, such as its location, who you were with, visual images of the various band members, the band’s sounds and so on. These different components need to be integrated, or linked together, in the hippocampus to form a single episodic memory. When the memory is formed, the different components will then be gradually transferred to cortical areas in the brain specialised in the long-term storage of that specific type of information. It is suggested that this can also explain why Molaison could retrieve old memories. The memories were located elsewhere in the cortex and had already been formed, with well-established circuits linking the components. Consequently, these old memories did not depend on the hippocampal area (Gluck, Mercado & Myers, 2008; Schacter, Gilbert & Wegner, 2009).

Role of the amygdalaThe amygdala (pronounced uh-MIG-duh-luh) is a small structure (about 1.5 centimetres long) located next to and interconnected with the hippocampus in the medial temporal lobe. Like most other brain structures, we have an amygdala in each hemisphere.

The amygdala plays crucial roles in processing and regulating emotional reactions, particularly strong emotions such as fear and anger. For example, your amygdala enables you to detect

Learning Activity 7.4Review questions1 What is the hippocampus and where is it

located?2 Who is H.M. and why is he well known to

memory researchers?3 List the STM and LTM memory impairments

experienced by H.M. after his surgery and what these indicate about the roles played and not played by the hippocampus in memory.

4 Listen to an authoritative 30-minute BBC radio report on H.M. The report includes interviews with H.M. and commentaries by his psychologists Brenda Milner and Susan Corkin. Case Study: HM—The Man Who Couldn’t Remember (August 11, 2010) at http://www.bbc.co.uk/programmes/b00t6zqv

5 Complete a version of the ‘Trace the Star’ task used by Brenda Milner to assess H.M.’s procedural memory. Go to the ‘Research Replication’ tab under ‘Brenda Milner’ at the following website devised by Milner: http://www.greatcanadianpsych.ca/Researchers.html

6 What does the H.M. case study suggest about where LTMs are stored in the brain? Explain with reference to the case study.

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Amygdala

Amygdala

Hippocampus Hippocampus

Figure 7.7 The hippocampus is crucial for LTM formation – but not all LTM types.

People (and animals) with damage to the hippocampus also tend to have trouble remembering the location of objects. This indicates that the hippocampus is also important for spatial memory, which is memory for the physical location of objects in space (see box 10.2 on page 380). In addition, through its interaction with the amygdala, the hippocampus plays an important role in linking emotion and memory.

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possible danger when approached by a snarling dog and to recognise fearful expressions in others from their facial expressions before they even say a word. The amygdala has memory functions as well. In particular, it is involved in the encoding and storage of memories that have a significant emotional component (sometimes called emotional memories). People and animals with amygdala damage show reduced ability to acquire conditioned (learned) emotional responses and to interpret or express a variety of emotions.

We are more likely to remember events that produce strong emotional reactions than events that do not. One reason is that the amygdala attaches emotional significance to this type of experience and stimulates the hippocampus to encode and store the relevant emotional details. In this way, the amygdala contributes to the formation of explicit declarative memories. This is apparent in a specific type of episodic memory known as a flashbulb memory.

A flashbulb memory is a vivid and highly detailed memory of the circumstances in which someone first learns of a very surprising, significant or emotionally arousing event; for example, when hearing about the unexpected death of an important person in their life or of a shocking incident that dominates the news. Many years later people can remember details about where they were, what they were doing, who they were with and what their emotional reaction was to the event. It appears that the level of emotional arousal at the time of encoding influences the strength of the long-term memory formed of that event. This is partly attributable to the increased amount of the neurotransmitter norepinephrine at the amygdala during times of heightened emotional arousal. It is believed that its presence may provide a signal to the hippocampus to ‘tag’ the memory of the event with important emotional details and strengthen its long-term storage. In this way, the amygdala interacts with the hippocampus to link emotion and memory (Paré, 2003; Phelps, 2004; Richter-Levin, 2004; Hamann, 2009).

The amygdala is particularly important for the learning and memory of fear responses involving implicit memory. Research evidence suggests that the amygdala attaches significance to previously ‘neutral’ events that become associated with

fear. In a typical experiment, rats are exposed to a specific stimulus such as blue light that is neutral—the light is ‘meaningless’ and does not produce any reaction by the rat. The light is then followed by an electric shock, which produces a fear response. Eventually, through pairing of the light and shock so that they occur at about the same time, the previously neutral light produces the fear response on its own. If one particular part of the amygdala is then damaged or removed, this interferes with the acquisition and expression of the fear response to the light alone learned during the experiment (LeDoux, 2000).

Research conducted with humans on this type of learned response, called a conditioned fear response, has obtained similar results. Conditioned emotional responses involve implicit memory because they occur involuntarily in the presence of a relevant environmental stimulus. There is no intentional conscious recall and the memory of the response can be observed through the actions associated with the response. We just ‘react’ immediately and consciously evaluate whether there is any actual danger afterwards.

Figure 7.8 Flashbulb memories are so named because of the photographic nature of the memory of the event. Many people report flashbulb memories for the emotionally charged event of the September 11, 2001, terrorist attack on the World Trade Center in New York.

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sensory information)

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Non-conditionedresponse

Implicit memory Explicit memory

Amygdala Hippocampus(influenced by amygdala)

UnconsciousNon-verbalEmotionalProcedural

ConsciousVerbal

CognitiveDeclarative

Emotional event

Figure 7.9 The amygdala plays a crucial role in encoding and storing memories that have a significant emotional component, such as an emotional experience involving a fear response. The amygdala is essential for implicit memory of a conditioned fear response, but can also contribute to explicit memory by influencing the activity of the hippocampus.

Box 7.2Research on the role of the amygdala in conditioned fear responsesOne of the best known studies with human participants was conducted by American psychologist Antoine Bechara and his colleagues (1995). The study involved three participants, each with significant brain damage:

• S.M., who had a damaged amygdala in each temporal lobe (called bilateral amygdala damage) but no damage to either hippocampus

• W.C., who had a damaged hippocampus in each temporal lobe (bilateral hippocampal damage) but no damage to either amygdala

• R.H., who had damage to each amygdala and

each hippocampus (bilateral amygdala and hippocampal damage). All three participants were shown a series

of coloured lights and each time a blue light was presented a loud, startling boat horn was sounded. After several presentations (i.e. trials), the blue light was presented alone and each participant’s ‘skin conductance response’ (i.e. GSR) was measured as an indicator of their level of conditioned fear.

The results are shown in table 7.1. When all participants were asked to report contextual information about what had happened during

People with damage to their amygdala are unable to acquire a conditioned fear response. These individuals form conscious explicit memories

involving details of the learning process but not implicit procedural memories that would enable them to produce the fear response (see box 7.2).

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Consolidation theoryResearch evidence suggests that new information transferred from STM (or working memory) to LTM requires a period of time for a process of consolidation to occur in order for it to be encoded and permanently stored. Consolidation theory proposes that structural changes occur in brain neurons when something new is being learned, and immediately after learning. These neuronal changes require a period after learning takes place, as the new information sets (‘consolidates’) in memory and becomes stable and enduring. The resulting structural changes in the neurons and their connections are said to form the long-term memory of what has been learned.

Consolidation theory also proposes that if memory formation is disrupted during consolidation, information may not be embedded in LTM and may therefore be lost. If disruption does not occur, the information will be permanently stored, at least until it is retrieved. Consolidation of information appears to be a gradual process, and the information being

Learning Activity 7.5Review questions1 Where is the amygdala located?2 What role(s) does the amygdala play in:

a implicit memory?b explicit memory?

3 Why are conditioned emotional responses said to involve implicit memory?

4 How does the hippocampus receive information about an emotional event from the amygdala?

5 What role does the hippocampus play in the formation of emotional memories?

6 Identify the independent and dependent variables in the study by Antoine Bechara and colleagues (1995).

7 Callie was badly bitten by her neighbour’s dog yesterday. Describe what would happen if Callie saw the dog today under each of the following conditions: a no amygdala or hippocampal damage b bilateral amygdala damagec bilateral hippocampal damage.

the experiment, only participant S.M., with amygdala damage, could accurately report details such as ‘A light comes on, followed by the horn’. However, S.M. failed to show a conditioned fear response when the blue light was presented alone, indicating that he had not acquired a conditioned fear response. In contrast, participant W.C., with hippocampal damage, showed a conditioned fear response to the blue light but could not remember and therefore report any

details of the experiment. Finally, participant R.H., with both amygdala and hippocampal damage, showed neither a conditioned fear response nor any recollection of the trials. The results of this study indicate that damage to the amygdala interferes with the acquisition of a conditioned fear response, providing evidence for the crucial role of the amygdala (but not the hippocampus) in acquiring and expressing a conditioned fear response (LeDoux, 2007).

Table 7.1 Results of experiment on conditioned fear response and recollection in participants with brain damage

Participant Conditioned fear response (procedural, implicit memory)

Conscious recollection of experiment (declarative, explicit memory)

S.M. (bilateral amygdala damage)

– +

W.C. (bilateral hippocampal damage)

+ –

R.H. (bilateral amygdala and hippocampal damage)

– –

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remembered is vulnerable to disruption for at least 30 minutes, although consolidation of memories can proceed for as long as several years in people and for weeks in lower-order animals, such as mice, rats and rabbits (Dudai, 2004; Breedlove, Rosenzweig & Watson, 2007).

The consolidation of information during transfer from STM to LTM can be compared to writing your name in wet concrete. Once the concrete has ‘set’ (the information consolidated in LTM), your name (the information) is relatively permanently ingrained. But while it is setting (the process of consolidation), it can be interfered with (altered) or erased (completely lost).

It is believed that the hippocampus plays a crucial role in consolidation. For example, surgical removal of the hippocampus in each temporal lobe to treat Henry Molaison’s epilepsy may explain why he was incapable of forming new long-term episodic or semantic memories. The process of consolidation was unable to occur due to the lack of structures that coordinate the ‘strengthening’ of the neurons and neural connections involved in the new memories (Gluck, Mercado & Myers, 2008; Schacter, Gilbert & Wegner, 2009).

Research on consolidation theoryEvidence in support of consolidation comes from studies of people who have experienced brain trauma resulting in memory loss; for example, after being knocked unconscious as a result of an accident, after acquiring certain diseases affecting the brain (such as encephalitis) or after receiving electroconvulsive therapy (ECT) as part of the treatment used in severe cases of depression (see box 15.5 on page 615). These people are frequently unable to report any memory of the events immediately before the accident or treatment, and in many instances they cannot remember anything that occurred during a period of about 30 minutes before the brain trauma (Squire & Kandel, 1999; Breedlove, Rosenzweig & Watson, 2007).

Other evidence for consolidation theory has come from research using animals. In one of the earliest and best known studies, researchers were interested in learning whether rats that were given ECT at various intervals after learning to run a maze would be able to remember the task they had

learned. American psychologist William Hudspeth and his colleagues administered ECT to the rats in group A immediately after they had learnt the task, to group B 20 seconds after learning, to group C 30 minutes later and to group D 60 minutes after learning. The results showed that consolidation of information occurred within about 60 minutes of the rats learning the task. None of the rats in group A remembered the task they had learned. Those in groups B and C showed partial retention (but group C’s retention was on average greater than group B’s). And all the rats in group D remembered the task completely (Hudspeth, McGaugh & Thomson, 1964).

ReconsolidationIt has been proposed that after a memory is activated and retrieved from LTM, it needs to be consolidated again in order to be stored back in LTM. This is process is known as reconsolidation.

According to American psychologists Michael Gazzaniga and Todd Heatherton (2006), evidence for reconsolidation has been obtained in studies with rats that were injected with drugs that interfered with memory storage after a memory had been activated. The rats were unable to reliably or accurately recall the information that was once stored in LTM. This suggests that memories for past events can be affected by new circumstances once they are retrieved, so that the newly reconsolidated memories may differ from their original versions. This is similar to what would happen if you took a book out of the library and some pages were torn out of the book before it was returned. The book that is placed back on the shelf is slightly different to the one that was taken out—the information contained in those torn-out pages is no longer available for retrieval. The reconsolidation process repeats itself each time memory is activated and placed back in storage, which may explain why our memories for events can change over time.

Reconsolidation theory has received considerable attention, because it not only has implications for what it means to remember something but also opens up the possibility that bad memories could be erased by activating them and then interfering with reconsolidation.

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structure or area of the brain associated with memory. The term brain trauma is an ‘umbrella’ term that refers to any brain damage that impairs, or interferes with, the normal functioning of the brain, either temporarily or permanently. The damage may be due to an inflicted brain injury caused by an intentional blow to the head

Box 7.3Brain trauma and memory lossIn some cases of serious car crashes and other events causing severe head trauma, the jarring of the brain can cause a loss of memory for events before and after the impact. Sometimes a person cannot remember whole days or months, particularly if they are unconscious for a time. Eventually, any permanent memory loss is usually confined only to the contents of STM during the time of the trauma since the information was never stored in LTM. This type of memory loss was evident in the case of a flight attendant who survived a fall from a Yugoslavian plane that blew up in the sky after a terrorist bomb exploded. The flight attendant suffered brain damage and spinal injuries and was paralysed from the waist down after falling more than 4000 metres. After regaining consciousness, she remembered boarding the plane and waking

up in the hospital, but could not remember any of the events in between (Loftus, 1980).

Activities such as boxing can also create brain trauma. Punches and other blows to the head can damage neurons and blood vessels in the fragile brain tissue, causing the ‘punch-drunk’ symptoms often seen in boxers. One study that examined the brain tissues of 15 boxers at autopsy found brain damage of the type that could interfere with memory processes in all of them (Corsellis, Bruton & Freeman-Brown, 1973).

Learning Activity 7.6Review questions1 Briefly describe consolidation theory.2 What three conditions are necessary for

memory to be consolidated and therefore permanently stored?

3 Use consolidation theory to explain why a rugby player who is knocked unconscious during a game may be unable to remember how he was knocked unconscious.

4 Give an example of research evidence for the hippocampus having a crucial role in consolidation.

5 Construct a research hypothesis for the experiment conducted by Hudspeth,

McGaugh and Thomson (1964). Ensure you operationalise the variables.

6 a Briefly describe reconsolidation theory.b Explain how reconsolidation may account

for retrieval of distorted memories.c Reconsolidation theory suggests that a drug

could be developed to erase unwanted or inappropriate memories. Suggest how a drug might be used for memory erasure with reference to reconsolidation theory.

d Give an example of an ethical issue that may be relevant to intentional memory erasure.

Amnesia resulting from brain trauma and neurodegenerative diseasesMany causes of memory failure or loss have a neurological basis, which results from some sort of damage or injury to the brain, usually in a specific

Figure 7.10 The boxer who received this blow may have sustained damage to fragile brain tissue that could interfere with memory processes. Years of this type of punishment can also lead to brain damage resulting in ‘punch-drunk’ behaviour.

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or by violent shaking of the head sufficient to rupture veins or cause some other kind of injury. Alternatively, the damage may be due to an acquired brain injury at some time after birth caused by an accident, a stroke, brain infection, long-term alcoholism, drug abuse, ECT, brain surgery or by a neurodegenerative disease of the brain (Brain Injury Australia, 2012).

A neurodegenerative disease is a disorder characterised by the progressive decline in the structure, activity and function of brain tissue. Essentially, neurons within the brain tissue (‘neuro’) gradually become damaged or deteriorate (‘degenerate’) and lose their function, hence the term ‘neurodegenerative’. With neurodegenerative diseases, the gradual deterioration is typically age-related. For example, Alzheimer’s disease is an age-related neurodegenerative disease linked to damaged neurons, resulting in memory failure and loss as well as a range of other problems. It is age-related because it is more common in older people and the problems usually worsen with age, particularly memory failure and memory loss.

Memory loss due to any reason is called amnesia. The term amnesia is used to refer to loss of memory, either partial or complete, temporary or permanent. Brain trauma caused by either an inflicted or acquired head injury commonly results in some kind of amnesia. The severity of the injury determines the specific characteristics of the amnesia. However, there is typically a temporary loss of consciousness followed by a period of confusion. The period forgotten generally reduces over time, often leaving some ‘residual’ amnesia of only a few seconds to a minute for events immediately preceding the injury. The duration of

the post-traumatic amnesia varies. For example, one study of patients with severe head injuries found that 10% of patients had durations of less than one week, 30% had durations of two to three weeks, and the remaining 60% had durations of more than three weeks (Whitty & Zangwill, 1966). Sometimes certain events, such as the visit of a relative or some unusual occurrence, are retained as ‘islands of memory’ during this amnesic period. Amnesia caused by a head injury commonly ends quite abruptly, often after a period of natural sleep (Kolb & Whishaw, 1996).

There are many different kinds of amnesia, each of which has a different pattern of symptoms. For example, case studies have been reported of people who become amnesic for the meaning of nouns, but not verbs, and vice versa. There are other case studies of people who become amnesic for animals, but not people, or who become amnesic for human faces but not for other objects. Sometimes only STM is affected, while in other cases people have difficulty learning new information or accessing information from LTM, or have no sense of the present.

Two types of amnesia, each of which is associated with different kinds of memory loss, are called anterograde amnesia and retrograde amnesia. We examine each kind of amnesia with reference to brain trauma and neurodegenerative diseases.

Anterograde amnesiaIf brain trauma causes loss of memory only for information or events experienced after the trauma occurs, it is called anterograde amnesia (antero means forward—in this case, forward in time). In general, the memory of information or events

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experienced prior to the trauma still remains. People with anterograde amnesia lose the ability to form or store new memories. They can talk about the things that happened before the onset of their amnesia, but they cannot remember what has happened since. Like H.M., they have difficulty learning new information such as the names of people they subsequently meet, regardless of how often they see them.

Anterograde amnesia is one of the symptoms experienced by people with Alzheimer’s disease or Korsakoff’s syndrome. Korsakoff’s syndrome is a neurodegenerative disease involving severe memory disorders associated with brain damage, particularly deep within the middle of the brain where the thalamus is located. Korsakoff’s syndrome occurs mainly in people who are chronic (long-term) alcoholics and is linked to the prolonged loss of thiamine (vitamin B) from their diets. Alcoholics who obtain most of their calories from alcohol and neglect their diet most often have this thiamine deficiency. Although Korsakoff’s syndrome is considered to be a neurodegenerative disease, the symptoms may appear suddenly within the space of days.

Someone with Korsakoff’s syndrome typically appears quite normal. They have relatively normal IQs, are alert and attentive, appear motivated, can

make witty remarks and play chess or a game of cards. However, many people with the disease have anterograde amnesia and therefore find it difficult or are unable to form new memories. Nor do they tend to be aware that they have memory problems. They often don’t remember new information for more than a few minutes; for example, they can read a magazine and, after a few minutes, read the magazine as if it were new. Sometimes someone with Korsakoff’s syndrome may forget what they’ve done an instant before. They may read the same page of a magazine over and over again, sometimes for hours, because they are absolutely unable to remember what they have read. Or, you might meet the person, have a conversation, go into another room for a moment and on returning observe that they will have absolutely no recollection that you had already met and spoken with them (Kolb & Whishaw, 1996).

People with Korsakoff’s syndrome may also have extensive loss of past memories (retrograde amnesia), particularly of their adult life. However, they can usually remember quite accurately the past events they experienced long before the serious onset of their disease, such as events that occurred during their childhood and adolescent years. It is often difficult for researchers and therapists to determine what someone with Korsakoff’s syndrome can and cannot truly remember. This is because it is quite common for someone with Korsakoff’s syndrome to confabulate. Confabulation involves filling in gaps in memory with plausible but untrue stories rather than admitting memory loss. This is often done confidently but occurs unintentionally as a result of confusing semantic and episodic memories (Stirling, 2002).

Not all people who are alcoholics develop Korsakoff’s syndrome. Treating a person with Korsakoff’s syndrome with a thiamine supplement can prevent further deterioration of memory functions, but it will not reverse the damage (Breedlove, Rosenzweig & Watson, 2007).

Retrograde amnesiaIf brain trauma affects memory for information or events experienced before the trauma occurs, it is called retrograde amnesia (retro means backwards—in this case, backwards in time). The memory loss may extend back a few moments,

Figure 7.11 The 2001 movie Memento with Guy Pearce in the lead role portrays anterograde amnesia. Anterograde amnesia involves loss of memory for information or events experienced after brain trauma occurs.

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07014

(a)

(b)

Old memories are lost New memories can be formed

Accident that causes amnesia occurs

Old memories remain New memories can’t be formed

Figure 7.13 (a) In retrograde amnesia, the person loses some or all memories formed before the brain trauma occurred; (b) in anterograde amnesia, the person cannot form new memories for events that occur after the brain trauma.

Figure 7.12 The 2002 movie The Bourne Identity with Matt Damon in the lead role portrays retrograde amnesia. Retrograde amnesia involves a loss of memory for information or events experienced before brain trauma occurs.

days, weeks or sometimes years. Retrograde amnesias are usually of a temporary nature and are often caused by a blow to the head, such as one received in a car accident, a boxing match or a sporting accident. Retrograde amnesia is also experienced by people with severe depression who have been treated by ECT (Andreasen & Black, 1996).

One case of retrograde amnesia was reported by English neurologist Ritchie Russell (cited in Baddeley, 1999). The case involved a 22-year-old greenkeeper who was thrown from his motorcycle in August 1933. There was a bruise in the left frontal lobe area and slight bleeding from the left ear, but no fracture was seen on X-ray examination. A week after the accident he was able to converse sensibly, and the nursing staff considered that he had fully recovered consciousness. When questioned, however, he said that the date was February 1922 and that he was a schoolboy. He had no recollection of five years spent in Australia, two of which were spent working on a golf course.

Two weeks after the injury he remembered the five years spent in Australia, and remembered returning to England, but the previous two years were a complete blank. Three weeks after the injury he returned to the village where he had been working for two years. Everything looked strange, and he had no recollection of ever having been there before. He lost his way on more than one occasion. Still feeling a stranger to the district, he returned to work. He was able to do his work satisfactorily, but he had difficulty in remembering

what he had actually done during the day. About ten weeks after the accident, the events of the past two years gradually returned and finally he was able to remember everything up to within a few minutes of the accident.

Typically, people who experience retrograde amnesia find that their inability to remember information and events leading up to the brain trauma gradually disappears. The period for which the memory is lost shrinks as the person gradually recovers their memory. However, people who have experienced retrograde amnesia typically find that their memory for the period immediately before the accident is never recovered.

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Dementia and Alzheimer’s diseaseDementiaDementia is an umbrella term used to describe a variety of symptoms of a large group of neurodegenerative diseases and other disorders that cause a progressive decline in mental functioning, behaviour and the ability to perform everyday tasks.

One of the main symptoms of dementia is memory loss. We all forget things from time to time, but dementia is different. For example, normal forgetfulness may include misplacing your sunglasses, but a person with dementia may lose their sunglasses and then forget what they’re used for. Other common symptoms include a decline in mental abilities such as reasoning, problem-solving and decision making, as well as behaviour and personality changes such as becoming more assertive, more withdrawn or less flexible, losing interest in things that have mattered previously, becoming absent-minded or repeating the same story or question. However, every individual experiences dementia in a different way and their experience depends on the type or cause of their dementia (Australian Institute of Health and Welfare, 2011; Dementia Care Australia, 2013).

Dementia is often described as progressing in stages, with memory loss typically being one

of the first signs of its onset. Memory loss is persistent rather than occasional and worsens as the dementia progresses. It may affect a person’s ability to continue to work or carry out familiar tasks. It may mean they have difficulty finding the way home. Eventually it may mean forgetting how to dress or how to bathe. With advanced dementia in the final stage, a person may become unable to care for themself and require the help of a carer or even full-time nursing.

Dementia mostly affects people over the age of 80 years, but it can have a younger onset and affect people in their 50s, 40s or even their 30s. It usually develops over a number of years, gradually worsening. However, dementia is not a normal part of the ageing process. Most people who age do not develop dementia. More than 100 known diseases, many of which are neurodegenerative, can cause dementia symptoms. When caused by neurodegenerative factors, the onset of the disease and its symptoms cannot be reversed.

An estimated 298,000 Australians had dementia in 2011, of whom 62% were women, 74% were aged 75 and over, and 70% lived in the community. Box 7.4 summarises some of the different types of dementia. The most common type is Alzheimer’s disease, accounting for about 50% to 75% of all dementia cases worldwide (Australian Institute of Health and Welfare, 2011).

Learning Activity 7.7Review questions1 What is amnesia?2 Explain the meaning of the phrase

‘amnesia resulting from brain trauma and neurodegenerative disease’.

3 Why are Alzheimer’s disease and Korsakoff’s syndrome considered to be neurodegenerative diseases?

4 Distinguish between amnesia that may result from an inflicted brain injury or from an acquired brain injury.

5 Distinguish between anterograde amnesia and retrograde amnesia, with reference to an example.

6 Voula was involved in a car accident as a passenger. She was not wearing a seatbelt and hit her head on the front windscreen when the two cars collided. She was unconscious for a short time. Brain scans showed there was no permanent brain damage; however, Voula experienced memory problems for some time after the accident.a If Voula suffered anterograde amnesia,

what memory problems is she likely to experience?

b If Voula suffered retrograde amnesia, what memory problems is she likely to experience?

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Alzheimer’s diseaseAlzheimer’s disease is a type of dementia characterised by the gradual widespread degeneration of brain neurons, causing memory loss, a decline in cognitive and social skills, and personality changes. In the early stages, short-term memory loss, apathy and depression are common.

Currently, Alzheimer’s disease is the fourth largest cause of death in Australia. It is estimated that more than 100 000 Australians suffer from Alzheimer’s disease. The disease is most common among older people with dementia, particularly among women. It affects one in 25 people over 60,

one in eight people over 65, and one in four people over 80. It also affects some people in their mid 50s (Australian Institute of Health and Welfare, 2011).

There is no single or simple diagnostic test for Alzheimer’s disease (or any other dementia). An accurate diagnosis can only be made after death when an autopsy involving microscopic examination of brain tissue is conducted. Because physical signs are not readily detectable in the living patient, a person’s memory, general knowledge, intellectual and personal skills and overall functional capacity are assessed. The assessment process often includes

Box 7.4Types of dementiaThere are many different types of dementia, each with different causes and overlapping symptoms. The most common types are described below.

Type of dementia Description

Alzheimer’s disease The most common type of dementia, it involves progressive degeneration of the brain’s neurons, resulting in loss of memory, impaired decision-making, confusion and personality changes. Accounts for about 50% to 75% of all dementia cases worldwide.

Vascular dementia Caused by problems of circulation of blood to the brain (e.g. can be brought on by a stroke). The second-most common type of dementia. Accounts for about 20% to 30% of all dementia cases.

Frontotemporal lobar degeneration (FTLD)

A group of dementias whereby there is degeneration in one or both of the frontal or temporal lobes of the brain.

Dementia with Lewy bodies

The name comes from the presence of abnormal spherical structures called Lewy bodies inside the neurons in the brain. This is caused by the degeneration and death of neurons. It is thought these may contribute to the death of brain cells. People with this type of dementia tend to have visual hallucinations or experience stiffness or shakiness, and their condition tends to fluctuate quite rapidly, often from hour to hour or day to day. These symptoms make it different from Alzheimer’s disease. Accounts for up to 5% of cases.

Parkinson’s disease A degenerative disease of the central nervous system, characterised by tremors, stiffness in limbs and joints, and speech impediments. Some people with Parkinson’s disease may develop dementia in the latter stages of the disease.

Korsakoff’s syndrome (alcohol-related dementia)

A dementia caused by long-term alcohol abuse, especially combined with a poor diet low in Vitamin B (thiamine).

Huntington’s disease An inherited, degenerative brain disease that affects the mind and body. It usually appears between the ages of 30 and 50, and is characterised by intellectual decline and irregular involuntary movements. Other symptoms include memory disturbance, personality change, slurred speech and impaired judgment. Dementia occurs in the majority of cases.

Source: Australian Institute of Health and Welfare (2011). Dementia in Australia. Canberra: Australian Institute of Health and Welfare. p. 2.

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input from others such as family members, carers and service providers. However, no one symptom is reliable, making diagnosis even more difficult (Alzheimer’s Australia, 2012).

In the initial stage of the disease, deficits are evident in a number of areas but the person can still function with minimal assistance. Moderate memory loss, especially for recent events, confusion, unusual irritability, impaired decision-making, reduced interest in hobbies and social activities, and needing to be prompted about personal care tasks are early symptoms of the disease. These continue to feature prominently as the disease progresses.

As well as experiencing a general decline in cognitive abilities, a person in the latter stages of the disease may be unable to recognise their own family members or regular carers, or may even forget their own identity (Baddeley, 1999). Severe personality changes are also associated with Alzheimer’s disease. For example, someone who was formerly quiet and polite may become obnoxious, swear a lot and continually make insulting sexual comments to friends and strangers alike. Alternatively, someone who was caring and outgoing may become apathetic and socially withdrawn.

Both the loss of past memories (retrograde amnesia) and difficulties in retaining newly learned information (anterograde amnesia) distinguish Alzheimer’s disease from many other disorders involving amnesia. Both declarative and procedural

memories are also impaired, gradually eroding as the disease progresses. Memory loss in the latter stages may include:

• events—forgetting part or all of a significant event such as a wedding and career

• words or names—forgetting words and names of well-known people and objects

• directions—inability to remember and follow written or verbal directions

• stories—inability to follow a story on television, in a movie or a book

• stored knowledge—forgetting known information such as historical or political information

• everyday skills—inability to perform tasks such as dressing, cooking, cleaning, using the toilet and taking medication.

Brain damage associated with Alzheimer’s diseasePostmortems of people who died with Alzheimer’s disease expose a brain with cortical areas that look shrivelled and shrunken due to the widespread death of neurons. The area of the brain that appears most affected is the medial temporal lobe, particularly the hippocampus. Autopsies have revealed that up to three-quarters of the neurons in this area may be lost in Alzheimer’s patients, and the remaining neurons are often damaged. This makes shrinkage in the hippocampal area especially severe.

Microscopic examination of neural tissue in a brain with Alzheimer’s disease usually reveals high levels of abnormal structures that interfere with neural communication within and between neurons, and therefore interfere with normal brain function. Amyloid plaques are fragments of the protein called beta amyloid that the body produces normally. In a healthy brain these protein fragments are broken down and eliminated from the brain naturally. In a brain with Alzheimer’s disease, the fragments accumulate over time to form hard, insoluble plaques outside and around the neurons, thereby inhibiting communication.

Within the neurons, another protein called tau also accumulates in an insoluble form. Gradually, the tau deposits form another type of abnormal structure called a neurofibrillary tangle. These tangles look like twisted fibres and inhibit transport of important substances from one part of the cell to

Figure 7.14 Because people with Alzheimer’s disease suffer severe memory impairment, they may benefit from a ‘structured environment’. For example, strategically placed labels enable this person to locate his personal belongings.

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Figure 7.15 (a) A PET scan of a normal brain. High levels of brain activity are indicated by the red and yellow areas. (b) A PET scan of a brain with Alzheimer’s disease. Note the reduced areas of activity compared to the scan of the normal brain. The lack of activity is most significant in the temporal and parietal lobes, which indicates their involvement in memory.

a b

Figure 7.16 Abnormal structures associated with Alzheimer’s disease that interfere with neural communication within and between neurons.

Normal Alzheimer’s disease

another. Both amyloid plaques and neurofibrillary tangles can occur as part of the normal ageing process of the brain, but they are much more abundant in individuals with symptoms of Alzheimer’s disease. It remains unclear whether these abnormal structures are causes or symptoms of Alzheimer’s disease.

The brains of people with Alzheimer’s disease also have greatly reduced levels of the neurotransmitter acetylcholine (ACh). The amount of ACh in the brain decreases naturally as we age. With Alzheimer’s disease, however, it decreases much quicker than normal. It is believed that the build up of amyloid and tau may contribute to this by destroying ACh-transmitting neurons.

There is no cure for Alzheimer’s disease. However, the use of medications that boost the level of ACh in the brain in the early or middle stages of Alzheimer’s disease can slow the rate of development of the symptoms. These drugs improve the efficiency of damaged neurons. Medications can also ease some of the ‘secondary’ symptoms of Alzheimer’s disease, such as depression.

Neuroimaging techniques such as CAT, PET and MRI can be used to identify the extent of brain damage resulting from Alzheimer’s disease. The resulting scans make it possible to identify the parts of the brain that have deteriorated. The images in figure 7.15 show the marked deterioration in brain areas associated with Alzheimer’s disease.

07019

Alzheimers disease

Neurofibrillarytangles

Amyloidplaques

Normal

Neuron

07019

Alzheimers disease

Neurofibrillarytangles

Amyloidplaques

Normal

Neuron

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Memory decline over the lifespanMany people believe that decline, or deterioration, of memory (and other mental abilities) occurs alongside the gradual decline in physical abilities that takes place as we get older. Memory decline is seen as a natural part of ageing in the same way as physical decline. A limited understanding of the changes in the brain as part of the normal ageing process and in age-related diseases such as Alzheimer’s disease reinforces this belief about memory decline. But does growing old necessarily mean a decline in memory?

Generally, results of research studies indicate that there may be some naturally occurring decline in some aspects of memory among older people; however, memory decline is not an inevitable consequence of ageing. The memory of some older adults can be as sharp as that of a 20-year-old. Others, however, experience memory impairments in one or more memory systems. If a decline in memory is experienced through ageing, effects are more likely to be experienced in short-term (working) memory and explicit declarative memories (mainly episodic) than in procedural memory.

Effects of ageing on short-term (working) memoryThe impact of age on STM seems to depend on the nature of the task. In general, if the task is relatively simple, such as remembering a list of words, STM is not affected by age. However, if the task is more complicated, requiring simultaneous storage and manipulation of information in working memory, or when attention must be divided between tasks, then age-related factors may impact on effective STM functioning (Whitbourne, 2001). For example, in one research study, older and younger participants were given a short list of unrelated words and asked to recall them in alphabetical order. This task involved both storage and manipulation of information. The mean recall for the younger participants was 3.2 correct words. For the older participants, the mean recall was 1.7 correct words (Craik, 1990).

These findings may have implications for the safety of elderly drivers. For example, keeping track of all the cars at a four-way intersection, deciding who has right of way and when they should enter the intersection is a complex working memory task. Retaining all the relevant information about each car’s location, recalling information from LTM to STM about relevant road rules and right of

Learning Activity 7.8Review questions1 Explain what dementia is with reference to

commonly described early and latter stage symptoms.

2 a What is Alzheimer’s disease?b Why is Alzheimer’s disease irreversible?c Why is Alzheimer’s disease attributable to

neurological factors?d Why does Alzheimer’s disease ultimately

lead to an earlier death?3 Consider the list on page 302 outlining

memory loss that can be experienced in the latter stages of Alzheimer’s disease. For each item in the list, identify thea specific type of LTM (e.g. semantic,

episodic, procedural)b LTM process (e.g. explicit or implicit

memory)c type of amnesia (e.g. retrograde or

anterograde).

Figure 7.17 Age may impact on effective STM functioning, especially if the task is complex. Driving involves simultaneously storing and manipulating information in working memory, which may explain why some elderly drivers are hesitant when they drive.

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way, and deciding when to enter the intersection requires both storage and manipulation of information simultaneously. This may explain why some elderly people are hesitant drivers.

Studies using neuroimaging techniques have shown that beyond 60 years of age, the activation of areas of the frontal lobes of the brain believed to be involved in STM decreases. In addition, the nervous systems of older people are less efficient at receiving and transmitting information, and therefore the rate or speed at which information is processed in short-term (working) memory is slower (Rypma & D’Esposito, 2000). In particular, as shown in figure 7.18, the ability of older people to process both numbers and words in STM seems to be less efficient (Salthouse, 1992).

Effects of ageing on long-term memoryAmerican psychologist K. Warner Schaie (1996) argues that researchers should not conclude anything about age-related LTM decline without clarifying the specific type of memory being discussed. Research findings indicate that some LTM types are more likely to be affected by age than others. For example, most studies of episodic memory have found a steady decline for memories of personal experiences as people age. Episodic memory can start to decline as early as age 30 or as late as age 50.

Swedish psychologist Lars-Goran Nilsson and his colleagues (1996) reported results from a longitudinal (long-term) study they conducted on age and memory, starting in 1988. This type of research involves studying an age-stratified sample of participants for an extended period and testing them periodically. Nilsson and his colleagues measured three types of LTM in 1000 randomly selected Swedes, ranging in age from 35 to 80, with 100 participants aged 35, 100 aged 40, 100 aged 45 and so on up to age 80. Their results showed the hypothesised age differences in episodic memories. The older participants performed worse than younger participants on 26 different measures of episodic memory. There was, however, hardly any decline in the retrieval of information from procedural memory. Procedural memories seemed to remain intact over time. Furthermore, semantic memory appeared to be fairly resistant to ageing as well. In some cases it actually improved for many older adults. The semantic memory tests used by Nilsson tapped general knowledge that most people would know regardless of their education.

Although many semantic and procedural memories are not easily lost, older people take longer to learn new information and skills—including information that would be stored as semantic and procedural memories respectively. It seems that older people do not encode new information with as much detail or as precisely as young people. Furthermore, the speed and fluency of retrieval of information from semantic memory particularly can decline with age (Baddeley, 1999). However, provided the information is well-learned and/or practised often, its maintenance in and retrieval from LTM is not necessarily affected as a result of age alone.

Psychologists have proposed several explanations for the memory changes that tend to occur as people age. One explanation is a lack of motivation. Older adults who have ‘seen the world’, established careers and raised families may have little or no interest in memorising apparently meaningless material such as nonsense syllables, word lists and number series typically used in a psychology experiment (Perlmutter, 1978). There is, however, less age-related decline in memory for tasks in which a person is motivated to remember

Figure 7.18 The effect of age on short-term (working) memory. The zero score on the y-axis represents the mean level of performance of younger research participants on both arithmetic and word tasks. As we age, our ability to process information is less efficient.

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to do something that is planned; for example, to take a cake out of the oven when it has baked, to take medication at the appropriate time or to attend a family celebration.

A second explanation is that as people get older they tend to lose confidence in their memory. When American psychologist Jane Berry and her colleagues (1989) gave research participants a test that measured their beliefs about their own memory skills, they found that 60- to 80-year-old adults were less confident than 18- to 30-year-olds (see figure 7.20). Memory of certain information may in fact decline at least slightly with age, but a lack of self-confidence can worsen the problem. The person who fears that they will not remember directions, an appointment or an old friend may not even try (Kassin, 1995).

A third explanation is that the inability of some older people to access information from LTM may be more to do with the kind of measure of retention used than with their age. For example, when research participants are asked to recall previously learned information, older participants perform significantly worse than younger participants. But when recognition is

used to measure retention of previously learned information, the difference in performance between older and younger participants is significantly less. Recall seems to be much more affected than recognition where the presence of retrieval cues

Figure 7.19 Losing confidence in one’s memory can be distressing.

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Figure 7.20 Participants were asked to rate how confident they were on a scale of 0–100 in their ability to perform various memory tasks. Older participants were consistently less confident than the younger participants.

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means much less effort is required to access the relevant information (Light, 1996).

In one study, American psychologist Harry Bahrick and his colleagues (1975) tested 392 adults ranging in age from 17 to 74 years to find out if they could remember the names and faces of their secondary school classmates. Some research participants had just finished secondary school, whereas others had finished up to 47 years earlier. The researchers found that participants became less able to recall names as they got older—even with the benefit of class photos as cues. But their ability to recognise names and photos or to match names and photos differed little in relation to age (see figure 7.21).

Probably the most widely researched hypothesis and explanation that accounts for most of the memory decline associated with age is the slowing of CNS functioning. As people age, their CNS functioning slows, and people are usually unable to mentally process information with the speed and efficiency that they once did. This slowing down of neural processes, called cognitive slowing, can impair performance in tasks involving memory as people age (Bashore, Ridderinkhof & van der Molen, 1997).

One explanation for cognitive slowing, especially in relation to memory processes, involves the frontal lobes. As a normal part of the ageing process, the size of the frontal lobes reduces. This shrinking is thought to be responsible for the many cognitive changes that tend to be experienced as

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Figure 7.21 A test of recognition showed little decline over time in participants’ ability to identify high-school classmates, even though they had left school 47 years before. A test of recall, however, showed a significant decline in their ability to remember the same names and faces.

Learning Activity 7.9Review questions1 Construct a table to summarise memory

decline associated with age in STM (working memory) and in the different types of LTM.

2 Use your table to write a one-paragraph description on age and memory decline.

3 What are four explanations of age-related decline in memory?

people age. These include memory decline and difficulties maintaining attention on a task for an extended period.

Research to test this explanation used neuroimaging to record frontal lobe activity while participants performed three different kinds of memory tasks. The first task involved recognition of previously learned words, the second involved recall of words previously learned and the third involved deciding whether what they had seen on a video was the same as a written description of the event. The results showed a consistent pattern. Older people whose frontal lobes showed reduced activity performed poorly on all three memory tasks compared with younger people. However, older people whose frontal lobes were highly active performed as well as young people on all three tasks (Roediger, 2003). Thus, it seems that the maintenance of cognitive abilities into old age may depend to some extent on the condition and functioning of the frontal lobes of the brain.

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Chapter 7 true/false quizIndicate whether each item is true or false by writing ‘T’ or ‘F’ in the blank space next to each statement.

1 ______ Memories are stored throughout the brain.

2 ______ Forgetting indicates that something is wrong with the brain.

3 ______ The amygdala interacts with the hippocampus in forming procedural memories.

4 ______ Dementia is an age-related disease.

5 ______ The amygdala has a role in both implicit and explicit memories.

6 ______ Alzheimer’s disease is neurodegenerative.

7 ______ Action potentials are received by dendrites and transmitted to the soma.

8 ______ The axon houses the cell’s nucleus.

9 ______ A synaptic gap is a component of the synapse.

10 ______ There is generally little change in recognition ability associated with ageing.

The answers to the true/false questions are in the Answers section on page 755.

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Section A—Multiple-choice questionsChoose the response that is correct or that best answers the question. A correct answer scores 1, an incorrect answer scores 0. Marks will not be deducted for incorrect answers. No marks will be given if more than one answer is completed for any question.

Q1 On recovering consciousness, a cyclist who was knocked unconscious in an accident is unable to recall events that occurred in the half hour or so before he was knocked out.

How would his amnesia be explained by consolidation theory?A lack of time for consolidation of

sensory information in short-term memory

B lack of attention during the half hour before the brain trauma

C lack of processing by the hippocampus in the parietal lobe

D lack of time for completion of changes in neurons involved in the formation of long-term memory

Q2 Dementia isA a normal part of ageing.B a form of Alzheimer’s disease.C a specific brain disease.D irreversible when neurodegenerative.

Q3 Long-term potentiation is best described asA the long-lasting strengthening of

synaptic connections resulting in enhanced functioning of neurons.

B the long-lasting release of neurotransmitter during memory formation.

C the formation of a long-term memory.

D the potential to form a long-term memory.

Q4 A neurodegenerative disease is best described asA a brain trauma.B an inflicted or acquired brain injury.C a brain-related disorder associated

with older people.D a progressive decline in the

structure and/or function of neurons in the central nervous system.

Q5 Research findings on the role of the neuron in memory indicate thatA there is an increase in the amount

of synapses produced by neurons, thereby enabling them to flow more freely within a memory circuit.

B when a memory is forming, new neurotransmitters grow and interconnect the neurons so that a memory circuit can be established.

C neurons change in structure and function when a memory is forming.

D neurons assemble in a formation that creates a memory circuit for the information.

Chapter 7 test

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Q6 Age-related decline in memory is more likely to be experienced with _____ memory.A semanticB workingC implicitD procedural

Q7 The amygdala is locatedA in the medial lobe.B next to the hippocampus.C in the cerebral cortex.D next to the temporal medial lobe.

Q8 During memory formation, neurons communicate with one another by sending _____ across the _____ .A neurotransmitter; synaptic gapB axon; synapseC synapse; synaptic gapD neurotransmitter; synapse

Q9 Consolidation of a memory involvesA memory loss or decline.B transfer to the hippocampus.C transfer from LTM to STM.D structural changes to neurons.

Q10 A neuron that receives neurotransmitter is called _____ and its receptors are found on a/an _____ .A presynaptic; dendriteB postsynaptic; axonC postsynaptic; dendriteD presynaptic; axon

The answers to the chapter 7 multiple-choice questions are in the Answers section on page 755.

Section B—Short-answer questionsAnswer all questions in the spaces provided.

Question 1 (1 mark)

Which neurotransmitter tends to be found in abnormally low levels among people with Alzheimer’s disease?

Question 2 (1 mark)

Loss of memory of events occurring before brain trauma is called __________________ amnesia, whereas loss of memory for events experienced after brain trauma is called __________________ amnesia.

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Question 3 (2 marks)

Describe two roles played by the hippocampus in memory formation.

Question 4 (4 marks)

Explain the role of the roles of the neuron and neurotransmitter as mechanisms of memory formation.

Question 5 (2 marks)

Draw a neuron and label four anatomical features.

The answers to the chapter 7 short-answer questions are available at www.OneStopDigital.com.au.

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