Neuronal signalling 2 Flashcards
membrane potential
the potential of the membrane of any cell
resting potential
membrane potential of a neurone not being stimulated
equilibrium potential
potential of the membrane for a single ion that stops further movement of that ion across the membrane
reversal potential
potential at which no further charge movement occurs across the membrane
for a single ion:
reversal potential = equilibrium potential
summation
- define
- what can this lead to?
the integration of many different EPSPs + IPSPs
when the integration is sufficiently excitatory to raise the membrane potential to threshold
- > Na+ channels open
- > action potential fired
2 mechanisms of summation
temporal
spatial
temporal summation
- define
- 2 effects
multiple stimulation at 1 synapse in a short period of time
a) graded potential doesn’t reach threshold so rapidly fades
- > cell returns to resting state
b) synapse releases neurotransmitters frequently in a short period of time
-> larger graded potential
= action potential
spatial summation
- define
- effects
simultaneous stimulation from 2+ nearby synapses (excitatory or inhibitory)
can have reinforcing or opposing effects
equal excitatory + inhibitory graded potentials
= cancel each other out
sequential opening of voltage-sensitive channels
-> leads to action potential
depolarisation above the threshold
-> massive opening of Na+ channels -> influx
= all or nothing spike
open K+ channels
= brief hyperpolarisation below resting potential
4 phases of an action potential
- Na+ channels open
-> influx
= depolarisation - K+ channels open
-> outflow
= repolarisation - Na+ channels inactive
-> refractory period
= hyper polarised - Na+ channels active, but closed
= returns to resting
2 types of refractory periods
absolute RP
= no further action potentials can be generated
relative RP
= more difficult, but some action potentials can be generated
restoration of the Na+ gradient
Na/K antiporter
exchanges 2 K+ from outside the cell
with 3 Na+ from inside the cell
using ATP
= Na+ pumped out of neurone
- > net movement of +ve charge
- > repolarisation
unequal distribution of Na+ and K+
membrane is more permeable to K+ than Na+
-> K+ diffuses in
Na/K pump moves Na+ out, K+ in
what does the Na/K anti porter maintain?
resting potential
returning to resting potential after an action potential
K+ channels close
repolarisation resets Na+ channels
ions diffuse away from area
Na/K antiporter maintains polarisation
what makes action potentials unidirectional?
Na+ channels go through brief inactive phases before closing
action potential cannot be fired again as the channels can’t be re-used
2 factors that ensure propagation
passive properties of an axon
(electronic spread)
Na+ channel excitability
action potential magnitude
all or nothing
- doesn’t vary in strength
passes undiminished as a wave along axon
action potential
- self-propagating
ion movement causes depolarisation
- > voltage-gated ion channels open
- > more Na+ ions move in
action potential sequence
- voltage-gated Na+ channels open
- Na+ influx
- at ~+40mV, Na+ channels close and K+ channels open
- outflow of K+ down electrochemical gradient
- K+ channels close
- K+ accumulates outside cell = depolarisation
- Na+/K+ antiporter repolarises
propagation movement
sodium ions passively diffuse along the axon
-> depolarises membrane
= opening on sodium channels
conduction velocity
large diameter axons
-> increases conduction velocity
myelinated neurones
- > passive spread of ions will activate channels only at Nodes of Ranvier
- > increases velocity
why myelinate a neurone?
increases conduction velocity
size requirement is diminished
electrical insulation
reduced cell-energy requirement
effect of myelin on neuronal size
an unmyelinated neurone would have to be 83x larger than a myelinated neurone to conduct the same speed
saltatory conduction
action potential jumps from 1 node to the next
-> travels faster than in an uncovered axon
neurotransmitters crossing the synapse
calcium entry causes release of neurotransmitters into the synaptic cleft
-> NTs bind to receptors on the post-synaptic membrane
role of calcium
calcium enters through VSCC
-> binds to calmodulin protein kinase
- > calmodulin phosphorylates synapsin I
- > synpasin I in phosphorylated form cannot bind to NT vesicles
- > vesicles can now be released in to synapse
how do action potentials cause neurotransmitter release?
neurotransmitters stored in synaptic vesicles
AP opens voltage-gated Ca2+ channels
-> Ca2+ ions cause vesicles to release contents at synapse
via exocytosis
3 types of calcium channels
what are they blocked by?
where are they found?
L-type
> 1,4-dihydropyridine
> skeletal muscle + cortex
N-type
> w-conotoxin
> CNS/PNS
P-type
> w-agatoxin
> cerebellum
types of neurotransmitters
acetylcholine
amines
(noradrenaline, dopamine, serotonin)
amino acids
(GABA, glutamate)
peptides
(endorphins, substance P)
synaptic transmission
- action potential arrives at presynaptic membrane
- depolarisation causes ca2+ influx
- Ca2+ promotes exocytosis of neurotransmitter
- nt binds to ion channels e.g. Na+
- EPSP spreads to spike initiation zone
- if depolarisation reaches threshold
- > spikes initiated in post-synaptic neurone
what is EPSP?
excitatory postsynaptic potential
neurotransmitter receptors
- what does nt binding cause?
- example of why some nts need to be degraded or cleared from the synapse?
- how is ACh removed?
-> change in membrane potential due to Ca2+ entry
glutamate can be toxic if not cleared
degraded by an enzyme
= ACh esterase
2 neurotransmitter receptor types
ionotropic
= ligand-gated ion channels
metabotropic
= linked to ion channels through G protein
(=GPCR)
ionotropic receptors examples
nicotinic acetyl-choline receptors
glycine
GABAa
metabotropic receptor examples
muscarinic acetyl-choline receptors
glutamate
GABAb
