Fig 2.9A simple sensory-motor (reflex) arc. A simple reflex is set in motion by a stimulus to the skin (or other part of the body). The nerve impulse travels to the spinal cord and then back out to a muscle, which contracts. Reflexes provide an “automatic” protective device for the body.

WITHOUT SYNAPSES NEURONS COULD NOT ‘TALK’ TO ONE ANOTHER AND WE WOULD HAVE NO BEHAVIOR

Interneuron SYNAPSES on motorneuron

Sensory neuron SYNAPSES oninterneuron

Receptor SYNAPSES on sensory neuron

Motor neuronSYNAPSES on muscle

Figure 3.4  Temporal and spatial summation

SYNAPSES

1. Structure of the synapseA. Presynaptic cell

1.Terminal button2. Synaptic vesicles3. Reuptake mechanisms

B. Synaptic cleftC. Post-synaptic cell

Postsynaptic membranes and receptors

SYNAPTIC TRANSMISSION

2. Types of synapses

A. axonal-dendritic (axon to dentrite)

B. axonal-somatic (axon to soma)

C. axonal-axonal (axon to axon –usually inhib)

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SYNAPTIC TRANSMISSION

3. Effects of presynaptic action potentials on polarization of post-synaptic cell

A. excitatory post-synaptic potential (EPSP)

B. inhibitory post-synaptic potential (IPSP)

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W. W. Norton

PRIOR TO RELEASE OF NT POSTSYNAPTIC CELL IS IN RESTING STATE AND POLARIZED AT –70mV

W. W. Norton

AFTER RELEASE OF NTs POSTSYNAPTIC CELL BECOMESDEPOLARIZED (LESS NEGATIVE) AND ONE CAN RECORDEXCITATORY POSTSYNAPTIC POTENTIALS. WHEN THESE ADD UP TO AT LEAST 10Mv AND ‘THRESHOLD’ IS REACHEDTHE POSTSYNAPTIC CELL WILL FIRE (ALL-OR-NONE)

W. W. Norton

?

W. W. Norton

Inhibitory postsynaptic potential

IF THE NT THAT IS RELEASED IS AN INHIBITORY NTIT PRODUCES GREATER POLARIZATION IN POSTSYNAPTIC CELLS AND ONE RECORDS IPSPs

SYNAPTIC TRANSMISSION

4. Summation of EPSPs and IPSPs on pos-synaptic cell by

A. temporal summation

B. spatial summation

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SYNAPTIC TRANSMISSION

5. Neurons synapse on one another and produce additive effects of EPSPs and IPSPs by

A. convergence

B. divergence

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Figure 2.1bAn example of a neuron, or nerve cell, showing several of its important features. The right foreground shows a nerve cell fiber in cross section, and the upper left inset gives a more realistic picture of the shape of neurons. The nerve impulse usually travels from the dendrites and soma to the branching ends of the axon. The neuron shown here is a motor neuron. Motor neurons originate in the brain or spinal cord and send their axons to the muscles or glands of the body.

SYNAPTIC TRANSMISSION

5. Neurons synapse on one another and produce additive effects of EPSPs and IPSPs by

A. convergence occurs when

B. divergence occurs when

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more than one axonterminates on a neuron

different axon terminals from a single neuron terminates ondifferent neurons

NEUROTRANSMITTERS

•Criteria for existence of neurotransmitter a. must be mechanisms in presynaptic cell for its      1. synthesis      2. storage      3. release 4. Inactivation

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Sequence of Events at a Synapse

Figure 3.8  Some of the major events in transmission at a synapse

Animation

Sequence of Events at a Synapse

Figure 3.8  Some of the major events in transmission at a synapse

Animation

?vesicles

cleft

Presynapticterminal

vesicles

Postsynaptic cell

1

2

3

4

55

6

synthesis

NEUROTRANSMITTERS

b. stimulation of the neuron must result in its release

c. must have specialized postsynaptic receptors

d. agonists will mimic and antagonists will block its effect

1. Criteria for existence of neurotransmitter

NEUROTRANSMITTERS

1. Different Neurotransmitters (and quick associations)

B. AminesDopamine (Parkinsonism, Schizophrenia, Reward)Norepinephrine (Learning, fear) Acetylcholine (Motor, memory, Alzheimers)Serotonin (Depression (SSRIs), aggression)

NEUROTRANSMITTERS

1.Different Neurotransmitters (and quick associations)

B. NeuropeptidesOpioids, endorphins (pain, addiction)CCK (satiation, eating)Oxytocin (milk-letdown, maternal behavior)GABA, Glutamate (inhibition, learning)

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DRUG EFFECTS ON NTS

3. Pharmacology

a.Agonists b.Antagonists

inhibitors, false transmitters, inhibitors of inactivation, depleting agents,etc.

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Synapses, Abused Drugs, and Behavior

How Drugs Affect Synapses

Agonist-a drug that mimics or increases the effects of a neurotransmitter

Antagonist-a drug that blocks or takes away from the effects of the neurotransmitter

Affinity-ability of a drug to bind a receptor

Efficacy-the degree to which the drug activates the receptor once bound

Figure 3.15  Events at a dopamine synapse

and how certain drugs affect the processDrugs can alter any stage of processing at a

synapse, from synthesis of the neurotransmitter through release and reuptake.

1.

2. 3

4.

5

Figure 3.15  Events at a dopamine synapse

and how certain drugs affect the processDrugs can alter any stage of processing at a

synapse, from synthesis of the neurotransmitter through release and reuptake.

1.AGO

2. ANTAG 3

4.

5 AGO

ANTAG

ANTAG

Dopamine is a neurotransmitter that excites postsynaptic neurons. If a drug were injected into an animal that blocked dopamine from attaching to its receptors, what would happen to the postsynaptic neurons?

Dopamine is a neurotransmitter that excites postsynaptic neurons. If a drug were injected into an animal that blocked dopamine from attaching to its receptors, what would happen to the postsynaptic neurons?

They would be less likely to produce further action potentials.

Parkinson’s Disease

Symptoms-rigidity, muscle tremors, slow movement, difficulty initiating movement

Brain Changes-Selective loss of cells in substantia nigra and amygdala/decrease in dopamine

Possible Causesgeneticsexposure to toxins (MPTP)smoking decreases risks/these data have been questioned

DISEASE CONDITIONS PRODUCED BY DISRUPTIONS INNEUROTRANSMISSION

Figure 8.16  Connections from the substantia nigra: (a) normal and (b) in Parkinson’s disease

Excitatory paths are shown in green; inhibitory are in red. The substantia nigra’s axons inhibit the putamen. Axon loss increases excitatory communication to the globus pallidus. The result is increased inhibition from the globus pallidus to the thalamus and decreased excitation from the thalamus to the cerebral cortex. People with Parkinson’s disease show decreased initiation of movement, slow and

inaccurate movement, and psychological depression.

BRAIN STRUCTURES THAT ARE DISRUPTED IN PARKINSON PATIENTS

Parkinson’s Disease

L-Dopa Treatment IS ONE treatment *precursor for dopaminedemonstrates individual effectivenessdoes not stop progression of the diseasenumerous side effects (nausea, restlessness, sleep problems, low

blood pressure, hallucinations, and delusions)

WHY the side effects?

*Therapies Other Than L-Dopaantioxidants, dopamine receptor stimulants, glutamate blockers,

neurotrophins, drugs that decrease apoptosis, pallidotomy, cell transplants

DRUG TREATMENTS FOR PARKINSON PATIENTS

BECAUSE DOPAMINE IS RELEASED AT MANY SYNAPSESALL OVER THE BRAIN AND PRODUCES EFFECTS SPECIFICTO THESE SITES.

ONE NOTABLE SIDE EFFECT OF L-DOPA (DA AGONIST) IS PSYCHOSIS

NOTE: SCHIZOPHRENICS WHO EXPERIENCE PSYCHOSIS ARE GIVEN NEUROLEPTICS WHICH ARE DOPAMINE ANTAGONISTS

ONE OF THE SIDE EFFECTS OF NEUROLEPTICS IS MOTORDISORDERS-TARDIVE DYSKINESIA

Drugs ‘of abuse’ have effects by acting on receptors in the brain

NicotineAttaches to nicotinic receptorsIncreases dopamine release in the nucleus accumbens

OpiatesDerived from opium poppyAttach to opioid receptors in the brainResult in increased dopamine release

PCPInhibits some glutamate receptorsResults in reinforcement in the nucleus accumbens

Marijuana/CannabinoidsBind to specific receptors in the brainLeads to euphoria

Other drugs of recreation

Hallucinogenic and stimulant Drugs (amphetamine, cocaine,etc.) Distort PerceptionMany resemble activities of neurotransmitters

CaffeineConstricts blood vessels in the brainInterferes with the effects of the neurotransmitter adenosine

(ANTAG)Alcohol-multiple effects on brain NTs

Inhibits flow of sodium across the membraneExpands the surface of membranesDecreases serotonin activity (ANTAG)Facilitates GABA responses (AGO)Blocks glutamate receptors (ANTAG)Increases dopamine activity (AGO)

Video

HORMONES AND BEHAVIOR

Hormones are chemicals secreted by endocrine organs in the body into the circulatory system

Hormones act at a distance from where they are releasedNTs act close to release point

Hormones act on receptors in other organs and in the brain

Hormones act on general metabolism, arousal, and growth

Hormones act in the brain to regulate behavior

WHAT ARE THE ENDOCRINE (HORMONE-PRODUCING) ORGANS ?

WHAT ARE THE ENDOCRINE (HORMONE-PRODUCING) ORGANS ?

1

2

3

WHAT ARE THE ENDOCRINE (HORMONE-PRODUCING) ORGANS ?

pituitary

adrenals

ovaries

Hormonal Changes Associated with the Menstrual Cycle in Women

Estrogen

Progesterone

Ovarian changes

LH and FSH from pituitary

follicular ovulation luteal

Age of onset of menarche in different cultures- Effect of diet?

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HORMONES also affect BEHAVIOR

Behaviors activated by hormones include

Sexual behaviorMaternal behaviorAggressionArousalEatingDrinkingLearning

Etc.

RAT SEXUAL BEHAVIOR-differences between males and females

Female sexual behavior activated by estrogen & progesterone

Method: baseline-ovariectomy-test-E&P-retestResult:behavior intact-eliminated-reinstated

Male sexual behavior activated by androgensMethod: baseline-castration-test-testosterone-test

Result: behavior intact-reduced-reinstated

Rat SEX

MaleMounts

Intromitsejaculates

FemaleHop-darts

Ear-wigglesLordosis reflex

IN HUMANS, ANDROGENS INFLUENCE MALE SEXUAL DESIRE

IN BOTH MALES AND FEMALES

WOMEN TREATED WITH ANDROGENS

WOMEN TREATEDWITH ESTROGENS

INTACT YOUNGERWOMEN,UNTREATED

WOMEN GIVEN PLACEBO

SEX DIFFERENCES IN ADULT BEHAVIOR ARE DUE TO

1. Differences in genes (XX,XY)2. Differences in prenatal hormone exposure3. Differences in upbringing4. Differences in cultural norms

All of which produce

1. Differences in brains2. Differences in hormones3. Differences in gender identity

HENCE-differences in feelings,attitudes, and behavior