Action potentials and synapses Flashcards by Lydia Brown

what is the resting membrane potential

potential difference across plasma membrane

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what is a normal resting membrane potential

-70mV

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how is a resting potential established

Na+/K+ ATPase pumps in neurone membranes pump 3Na+ out for every 2K+ in
Membrane more permeable to K+ than Na+
Equilibrium reached at resting potential

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why is there a difference in membrane permeability to Na+ and K+ in resting potential

Few VG Na+ channels open so relatively impermeable to Na+

VG K+ channels closed but leak K+ channels are open so membrane more permeable to K+

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Describe an AP in a post-synaptic membrane

NT binds to specific ligand gated ion channels so Na+ enters and initial depolarisation occurs
VG Na+ channels open so further depolarisation
Critical threshold potential reached and depolarisation becomes positive feedback
reverse polarization reached so VG Na+ inactivated
sluggish VG K+ channels open so rapid repolarisation
VG K+ close slowly so hyperpolarisation
RP restored when VG K+ close

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what is the approximate value of the critical threshold potential

-55mV

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what is the critical threshold potential

when depolarisation becomes a positive feedback loop; Na+ entry causes depolarisation which means more VG Na+ channels open etc

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what is the approximate value of the reverse polariszation

+30mV

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why do VG K+ channels open

in response to initial depolarisation but are sluggish to open initially

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why does hyperpolarisation occur

VG K+ channels close when negative potential reached but close slowly so continued outflow of K+

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what is the absolute refractory period

when VG Na+ channels are already open/ inactivated after 1st AP
- no second AP can be produced regardless of strength of stimulus

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what is the relative refractory period

2nd AP can be produced

needs much stronger stimulus
lasts until membrane resturns to resting potential

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how are AP propagated

AP generation causes current to flow which depolarises adjacent membranes to threshold potential and causes Na+ channels to open so propagation occurs

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what does propagation speed of AP depend on

fibre diameter and myelination

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why does increasing fibre diameter increase propagation speed of AP

less internal resistance to local current

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what is axonal transmission

transmission of information from A to B

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What is synaptic transmission

integration/ processing of information

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what is the pathophysiology of multiple sclerosis

degradation of myelin and development of scar tissue that eventually blocks neurotransmission along myelinated axons

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what are the symptoms of multiple sclerosis

uncontrolled eye movements
slurred speech
partial/ complete paralysis
tremor
loss of co-ordination 
weakness
sensory numbness
prickling 
pain

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who is most commonly affected by multiple sclerosis

young adults

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what is a synapse

specialised junction between 2 neurons where electrical activity in presynaptic neurone influences electrical activity of post-synaptic neurones

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what is an excitatory synapse

membrane potential of postsynaptic membrane is brought closer to threshold

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what is an inhibitory synapse

membrane potential of postsynaptic neurone hyperpolarised (brought further from threshold) or stabilised at resting potential

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what are the 2 types of synapses

electrical and chemical

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describe electrical synapses

gap junctions join plasma membrane of pre and post synaptic cells so local current flow directly very rapid - synchronised transmission

where are electrical synapses found

brainstem neurons and hypothalamus

describe the structure of chemical synapses

plasma mmebranes joined by synaptic cleft that prevents direct propagation of current presynaptic membrane has axon terminal synapses covered in astrocytes

what is contained in an axon terminal

synaptic vesicles that store neurotransmitter molecules

what is the name of additional neurotransmitters in a chemical synapse

co-transmitter

what do astrocytes in chemical synapses do

reuptake of excess neurotransmitter

Describe synaptic transmission at a chemical synapse

- AP causes VG Ca+ channels in pre-synaptic terminal to open - vesicles move, fuse and release contents - NT diffuses across cleft - attach to receptor sites on post-synaptic membrane

what are receptors for neurotransmitters

transmitter-gated ion channels | - specific

describe excitatory channels in chemical synapse

excitatory post-synaptic potential (EPSP) leads to depolarisation - many Na+ leave, few K+ enter

describe inhibitory channels in chemical synapses

inhibitory post-synaptic potential (IPSP) leads to hyperpolarisation - many K+ leave OR many Cl- enter

what are the 3 ways unbound neurotransmitters are removed from synaptic cleft

Reuptake Diffuse away Enzymatically transported into inactive substances

describe reuptake of NT in chemical synapse

active transport of NT back into presynaptic axon terminal/ nearby glial cells

what are the 5 processes of synaptic transmission

``` manufacture storage release interact with post-synaptic receptors inactivation ```

what is temporal summation

input arrives from same pre-synaptic cell at different times - potentials summate because greater number of open ion channels means increased flow of positive ions into cell

what is spatial summation

2 inputs occur at different locations in post-synaptic neurone

what are the 2 classes of neurotransmitters

fast and neuromodulators

describe fast neurotransmitters and give some examples

short lasting effects involved in rapid communication ACh, GLU, GABA

what do neuromodulator neurotransmitters do

cause changes in synaptic membrane

describe neuromodulators and give some examples

longer lasting involved in slower events (e.g. learning, development, motivational status) Dopamine, noradrenaline, serotonin

what are the most common local anaesthetics

procaine and lignocaine

what do local anaesthetics do

interrupt axonal transmission and block Na+ channels so prevent depolarisation so no AP generated

why do local anaesthetics generate pain relief

pain isn't transmitted

name 6 neurotransmitters

ACh, Noradrenaline (NA), dopamine (DA), serotonin, glutamate, GABA

Acetylcholine; - what neurones release it - what enzyme degrades it - what are the receptors - what is an example of an agonist

cholinergic neurons acetylcholinesterase nicotinic and muscarinic receptors nicotine is an agonist

describe what AChe does

breaks down ACh to acetate and choline; | choline is transported back into presynaptic axon terminal and reused to resynthesise ACh

describe nicotinic receptors

respond to ACh and nicotine contain ion-channels in neuromuscular junctions and brain

describe muscarinic receptors

respond to ACH receptor coupled with G proteins - alter activity of different enzymes/ ion channels in brain and junctions where major PNS divisions innervate peripheral glands/ organs

give some specific examples of muscarinic receptors

M2 - heart | M3 - bronchoconstriction

what does sarin do

inhibits ACHe causes build up of ACh in synaptic cleft overstimulation of ACh receptors leads to uncontrolled motor contractions eventually resulting in receptor desensitisation and paralysis

where is noradrenaline found

peripheral heart and CNS

what breaks down noradrenaline

monoamine oxidase (MAO)

what affects noradrenaline

antidepressant drugs, stimulants like amphetamine

what does amphetamine do

increases release of noradrenaline and blocks its reuptake

where is dopamine found

basal ganglia

what is the pathway of dopamine production

tyrosine converted to L-dopa which is decarboxylated to form dopamine

where does dopamine work

G-protein coupled receptors

how is dopamine removed from synaptic cleft

dopamine transporter

what affects dopamine

antipsycotic drugs, stimulants, anti-Parkinson's drugs

describe anti-Parkinson's drug

L-dopa increases dropamine manufacture; is dopamine precursor that is able to cross BBB - is taken up by serotonin neurons where it is converted and released as dopamine

where does serotonin act

excitatory effect on pathways that mediate sensation

what affects serotonin

antidepressants | ecstasy

what is the effect of ecstasy (NT)

neurotoxic to serotonin neurons

what is glutamate

main excitatory neurotransmitter

what is GABA

main inhibitory neurotransmitter

what does GABA stand for

gamma-aminobutyric acid