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Introduction to biological psychology. Topic 2: Structure and function of neurones. Properties of Neurones. In common with other cells : Cell membrane Nucleus : containing DNA, the genetic blueprint for the structure and function of the cell - PowerPoint PPT Presentation
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Introduction to biological psychology
Topic 2:Structure and function of neurones
Properties of Neurones
In common with other cells :
• Cell membrane
• Nucleus : containing DNA, the genetic blueprint for the structure and function of the cell
• Organelles and machinery for translating genetic code into proteins (Golgi apparatus, endoplasmic reticulum, ribosomes)
• Therefore structural and metabolic proteins (e.g. enzymes)
• Metabolic machinery enabling glucose oxidation to provide energy
Neuronal Specialisation
Excitability of the membrane
Dendrites – network of fine processes derived from cell body
Synapse – connection between two neurones
Axon – elongated neural process, specialised for rapid signal transmission over long distances
Myelination – fatty sheath round axon
Axon hillock – site of action potential generation
Membrane potentials
• The neuronal cell membrane is differentially permeable to intracellular and extracellular chemical constituents.
• Some ions can pass through the membrane easily, others can pass through, but with difficulty, others cannot pass through at all
• As a result of this differential permeability to ions, there is an uneven distribution of charge across the membrane
• This difference is the membrane potential: the resting membrane potential of neurones is around –70mV
• The main ions contributing to the membrane potential are positively charged sodium (Na+) and potassium (K+), and negatively charged chloride (Cl-) and proteins (A-).
Membrane potential
A-
K+
Na+
Cl-
-70mV
Inside Cell
A-
K+
Cl-
Na+
K+
Cl-
Na+
Outside Cell
Resting Potential = approx -70 mV
Changes in membrane potential
• Incoming signals cause changes in the dendritic membrane potential, by altering the permeability of the membrane to ions
• Increasing the permeability to chloride (Cl-) causes the membrane potential to become more negative (hyperpolarisation)
• Increasing the permeability to sodium (Na+) causes the membrane potential to become less negative (depolarisation)
Inside Cell
A-
K+
Cl-
Na+
K+
Cl-
Na+
Outside Cell
Na+Na+
Cl-Cl-
Signal transmission in dendrites
• Changes in charge diffuse passively along the membrane from the point of origin
• Relatively slow• Decay over distance
At any one point the membrane potential is determined by the sum of all the individual depolarising and hyperpolarising events originating nearby
Na+
+ + + +_
• The action potential then propagates the electrical signal along the axon
Pot
enti
al(m
V)
0
-50
-70
Time
The axon hillock
Axon hillock - the point where the axon leaves the cell body
• Specialised for the generation of action potentials• When the net depolarisation at the axon hillock reaches the threshold potential (around –50mV), an action potential is generated
No action potentialStill no action potential
Action potential
Pot
enti
al(m
V)
0
-50
-70
Time
30
The action potential
• ‘All-or-none’ phenomenon • an action potential is always the same size
• Does not decay over distance• an action potential is the same size when it reaches the terminal as it was when it left the axon hillock.
An electrical ‘spike’ caused by reversal of membrane polarity
• Mediated by rapid changes in membrane permeability to sodium and potassium
1 m sec
Refactory period
Conduction velocity in axons
Comparison of different classes of primary afferent axon
A-alpha fibre
A-beta fibre
A-delta fibre
C fibre 0
100
200
300
400
500
C fib
reW
alkin
gM
ileSp
rinter
a-de
lta Fast
Grey
houn
dCh
eetah
Mot
orwa
yAs
ian sw
iftA-
beta
Aero
plan
eA-
alpha
Spee
d (m
iles
per
hou
r)
The synapse
Vesicles containing neurotransmitter
Postsynaptic receptors
Neurotransmitter reuptake sites
Neurotransmitter released into synaptic cleft
Neurotransmitters
• Synthesised in the neurones, close to the site of release
• Stored on the terminal until required for release
• Released into synaptic cleft in response to an action potential
• Binds to receptors in post-synaptic membrane
• Causes changes in membrane potential
• Excitatory receptors cause depolarisation
• Inhibitory receptors cause hyperpolarisation
Examples of neurotransmitters
Type Transmitter Action
Amino acid Glutamate Excitatory (NMDA-type, AMPA-type receptors)
GABA Inhibitory (A-, and B-type receptors)
Monoamines Dopamine Excitatory (D1 & D5 receptors)Inhibitory (D2, D3 & D4 receptors)
Noradrenaline Excitatory (subtypes of alpha- & beta-receptors)Inhibitory (subtypes of alpha- & beta-receptors)
Serotonin Excitatory (5HT-1, 5HT-2 & 5HT-3 receptors) (= 5-hydroxytryptamine = 5HT) Inhibitory (some subtypes of 5HT-1 receptors)
Others Acetylcholine Excitatory (muscarinic & some nicotinic receptors)Inhibitory (subtypes of nicotinic receptors)
Synaptic transmission
Presynaptic neurone Synaptic cleft Postsynaptic neurone
neurotransmitterrelease
receptors
Chemical
Neurotransmitter
Electrical
Action potential
Electrical
Change in membrane potential
neurotransmitterrelease
receptorsreceptors
Reuptake and/or breakdownof neurotransmitter
receptors
Neurotransmitter-receptor interaction
Excitationor
Inhibition
Neurotransmitter
Receptor
AMJ Young, Jan, 2000C:\0_TEACH\PS103\lec2-sli.ppt
Changes in membrane potential
Receptor pharmacology
Neurotransmitter
Receptor
Excitationor inhibition
Neurotransmitter
Receptor
No effect
Receptor
Same action asnative transmitter
NeurotransmitterBinds to receptor and evokes excitation or inhibition
AgonistBinds to receptor and evokes the same response as the native transmitter.
AntagonistBinds to receptor and does not evoke any response.
Prevents the native transmitter or any agonist from binding to the receptor
Action potential Neurotransmitter Change in membrane potential
Reuptake and/or breakdownof neurotransmitter
Drugs affecting synaptic transmission
neurotransmitterrelease
receptors
Drugs affecting action potentials
Receptor agonistsand antagonists
Drugs affecting Synthesis & release
Drugs affecting reuptakeor breakdown
Drugs affecting membrane potentialDrugs affecting action potentials
Receptor agonistsand antagonists
Drugs affecting Synthesis & release
Drugs affecting reuptakeor breakdown
Drugs affecting membrane potential
Actions of therapeutic drugs
Synthesis Release Receptor Clearance
NT NT NT
TryptophanL-DOPA
Amantidine NeurolepticsAnxiolyticsAnticonvulsants
Tricyclic antidepressantsGABA-t inhibitors
Drugs acting atneurotransmitter receptors
• Many venom toxins• bungarotoxin (from cobras) : antag at acetylcholine receptors
• Neuroleptics (antipsychotics) – antagonist at dopamine receptors• Barbiturates and benzodiazapines (anticonvulsants, anxiolylics)
• increase GABA receptor function (allosteric binding site)
• Many plant derivatives • curare (from frogs) : antagonist at acetylcholine receptors• atropine (belladonna : from deadly nightshade) : antagonist at acetylcholine receptors : first pharmacological treatment for Parkinson’s disease• nicotine (from tobacco) : agonist at acetylcholine receptors• muscarine (from fungus) : agonist at acetylcholine receptors
Drugs affecting membrane potentials
Local anaesthetics• bind to ion channels in membrane, preventing changes in membrane potential
Puffer fish venom toxin (tetrodotoxin)• blocks voltage-dependent sodium channels, therefore blocks action potentials
Arrow frog venom toxins (batrachotoxin)• open voltage-dependent sodium channels, therefore “over excite” neurones
Drugs affecting neurotransmitter
synthesis and storage
Reserpine • prevents vesicular storage of amine transmitters
L-DOPA • precursor for dopamine – increases dopamine concentrations: main therapeutic agent used in Parkinson’s disease
Tryptophan• precursor for serotonin : effective in treating some depression
Drugs affecting neurotransmitter release
Black widow venom toxin• increases then eliminates acetylcholine release at NMJ
Botulinum toxin• Prevents acetylcholine release at neuromuscular junction (NMJ)
? Amantidine ?• Mechanism uncertain, but may increase dopamine release: used in the treatment of Parkinson’s disease
Drugs affecting reuptake and breakdown of neurotransmitters
Monoamine reuptake inhibitors• tricyclic antidepressants : prevents reuptake of noradrenaline and serotonin• fluoxitine (Prozac) : prevents reuptake of serotonin
Monoamine oxidase inhibitors• prevent the breakdown of amine neurotransmitters
• Selegiline (deprynil) : blocks dopamine breakdown: used in the treatment of Parkinson’s disease• Phenelzine : blocks breakdown of noradrenaline and serotonin: antidepressant
Amphetamine and cocaine• Increase dopamine levels by blocking reuptake: amphetamine also increases dopamine release and blocks monoamine oxidase
GABA transaminase (GABA-t) inhibitors• prevent the breakdown of GABA : anticonvulsant