Action potentials and synapses Flashcards
what is the resting membrane potential
potential difference across plasma membrane
what is a normal resting membrane potential
-70mV
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
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+
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
what is the approximate value of the critical threshold potential
-55mV
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
what is the approximate value of the reverse polariszation
+30mV
why do VG K+ channels open
in response to initial depolarisation but are sluggish to open initially
why does hyperpolarisation occur
VG K+ channels close when negative potential reached but close slowly so continued outflow of K+
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
what is the relative refractory period
2nd AP can be produced
- needs much stronger stimulus
- lasts until membrane resturns to resting potential
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
what does propagation speed of AP depend on
fibre diameter and myelination
why does increasing fibre diameter increase propagation speed of AP
less internal resistance to local current
what is axonal transmission
transmission of information from A to B
What is synaptic transmission
integration/ processing of information
what is the pathophysiology of multiple sclerosis
degradation of myelin and development of scar tissue that eventually blocks neurotransmission along myelinated axons
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
who is most commonly affected by multiple sclerosis
young adults
what is a synapse
specialised junction between 2 neurons where electrical activity in presynaptic neurone influences electrical activity of post-synaptic neurones
what is an excitatory synapse
membrane potential of postsynaptic membrane is brought closer to threshold
what is an inhibitory synapse
membrane potential of postsynaptic neurone hyperpolarised (brought further from threshold) or stabilised at resting potential
what are the 2 types of synapses
electrical and chemical
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
