PHYS: Action Potentials + Synapses Flashcards

(44 cards)

1
Q

what is resting membrane potential (RMP)

A
  • difference in electrical charge inside vs outside cell (-70mV) @ rest - polarised (charged)
  • inside is 70mV more negative than the outside due to -vely charged proteins in the cell
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2
Q

3 factors which influence RMP

A
  • concentration gradient b/n ECF (Na+, Cl-, Ca2+) and ICF (K+ and -ve proteins)
  • electrical gradient (all ions)
  • permeability of membrane
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3
Q

2 types of membrane ion channels (with conc grad)

A
  • leaky channels: open and close randomly = unregulated ion leakage (main contributor to RMP)
  • gated channels: open in response to a stimulus e.g. voltage, mechanical or chemical (ligand)
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4
Q

2 types of ion transporters (against conc grad)

A
  • ATPase pumps e.g. Na+/K+ pump or Ca2+ pump
  • ion exchangers e.g. Na+/Ca2+ exchanger
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5
Q

permeability of plasma membrane at rest

A
  • most permeable to K+
  • still permeable to Cl- and Na+
  • impermeable to -vely charged intracellular proteins
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6
Q

what is equilibrium potential

A
  • measure of membrane potential that counterbalances conc grad for one or more ion/s
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7
Q

how to calculate equilibrium potential with one ion

A
  • Nernst equation
  • E(ion) = electrical potential for ion (mV = millivolts)
  • Z = CHARGE of ion (1 for Na+ and K+, -1 for Cl-)
  • Co = conc of ion outside cell (mmol/L)
  • Ci = conc of ion inside cell (mmol/L)
  • outside and inside are reversed for anions
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8
Q

how do we know that the cell membrane is more permeable to K+ than Na+?

A
  • net movement down conc grad (Na+ in and K+ out) via leaky channels
  • E(K+) is larger than E(Na+) which means there are more leaky channels for K+
  • leak counterbalanced by active Na/K pump
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9
Q

sodium potassium pump

A
  • maintains RMP: actively counterbalances rate of Na+ and K+ leakage therefore no net movement of ions
  • 3 Na+ out and 2 K+ in
  • generates -1mV of potential (no role in generating AP)
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10
Q

how to calculate equilibrium potential w/ multiple ions

A
  • Goldman-Hodgkin-Katz equation (expanded version of Nernst)
  • each concentration is multiplied by its relative permeability
  • inside and outside for Cl- are reversed b/c anion
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11
Q

what is an action potential and how is it initiated?

A
  • rapid series of changes in RMP
  • may possibly take many sub-threshold stimuli to reach threshold
  • once threshold (-50 to -55 mV) is reached by a supra-threshold stimulus, action potential fires
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12
Q

polarisation

A

when there is a difference of charge in ECF and ICF (+ve or -ve)

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13
Q

resting state

A
  • neuron not transmitting action potential
  • RMP: -70 mV
  • Na+ and K+ channels closed
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14
Q

what is the threshold for an action potential and what does this mean in terms of ion flow?
- also what are 2 ways to reach the threshold?

A
  • -50 to -55 mV
  • point where enough voltage-gated Na+ channels have opened to balance the leakage of K+ ions out
  • 2 ways to reach threshold (summation): temporal (same neuron successively firing) or spatial (several neurons firing)
  • all or nothing response
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15
Q

depolarisation

A
  • Na+ ions come in due to opening of Na+ channels
  • ICF becomes more positively charged
  • K+ channels closed
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16
Q

repolarisation

A
  • charge returns to RMP after depolarisation
  • Na+ channels inactivated and K+ ions start to move
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17
Q

hyperpolarisation

A
  • K+ goes out due to opening of K+ channels
  • Na+ channels begin to reset and close
  • cell becomes more negative and then slowly returns to RMP
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18
Q

action potential stages

A
  • resting > threshold > depolarisation > depolarisation > hyperpolarisation > rest > refractory
19
Q

what is a graded potential?

A
  • smaller, localised changes in RMP
  • caused by opening of gated ion channels (voltage, ligand, mechanical)
  • ‘graded’ = have varying magnitudes based on size of stimulus whereas AP = all or nothing
  • spread bidirectionally unlike action potentials
  • slower and die out with distance b/c leakage of ions causes loss in current
  • can trigger APs in surrounding membranes
  • occur @ diff sites than APs
20
Q

equilibrium potential of Na+ and K+

A
  • Na+ = +60mV
  • K+ = -90mV
21
Q

states of Na+ voltage-gated channels

A
  • closed (resting phase): can open if there’s a big enough stimulus
  • opened by activation gate (depolarisation): Na+ can enter
  • inactivated (cannot open regardless of stimulus) - blocked by inactivation gate (repolarisation)
22
Q

states of K+ voltage-gated channels

A
  • closed (resting phase)
  • opened (depolarisation): K+ can exit
23
Q

absolute vs relative refractory period

A
  • absolute: when another AP cannot be elicited no matter the stimulus (usually during repolarisation b/c Na+ channels are inactivated and haven’t reset yet - unable to open)
  • relative: when AP can be elicited but with a stronger stimulus (usually when K+ channels are open during hyperpolarisation and start of rest)
24
Q

where is an AP generated and why?

A
  • initial origin site (axon hillock)
  • highest proportion of sodium channels so lowest threshold needed to produce an AP
25
two modes of conduction of an AP
- contiguous conduction (unmyelinated): spread along every patch of membrane down the length of the axon - saltatory conduction (myelinated): AP jumps over nodes of Ranvier
26
is myelin part of the neuron?
- no - separate schwann cells / oligodendrocytes wrap around the axon
27
2 factors which influence speed of AP propagation
- diameter of axon: larger axons are faster but take up more space - degree of myelination: ions can't penetrate lipids so acts as insulation to speed up transmission
28
demyelinating diseases of CNS and PNS
- CNS: MS - PNS: Guillain-barre syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP)
29
2 types of synapses
electrical and chemical
30
electrical synapse
- ions flow passively via gap junctions - bidirectional transmission (very small delay) - only between neurons - useful for quick, coordinated movements - shorter distance - e.g. burst of hormone secretion, CNS and heart
31
chemical synapse
- neurotransmitters released from presynaptic neuron via exocytosis (chemical messengers) - main mechanism of synaptic transmission - slower, unidirectional transmission - can be to other neurons or to effector cells (e.g. muscles) - CNS and PNS - longer distance
32
process of chemical synaptic transmission
- action potential arrives @ axon terminal > depolarisation - voltage-gated Ca2+ channels open > influx of Ca2+ ions - vesicles release NTs into synaptic cleft via exocytosis - Ca2+ is removed from axon terminal - either taken up by mitochondria OR ejected from neuron via active Ca2+ pump - NT diffuses across synaptic cleft and binds to specific receptor on postsynaptic neuron, opening ion channels which causes a GP - postsynaptic neuron is either excited or inhibited based on which receptor the neurotransmitter binds to
33
why is there a chemical synaptic delay?
- takes time for neurotransmitter to be released, diffuse across synaptic cleft and bind to receptors on PSN
34
CNS neurotransmitters
- excitatory: glutamate - inhibitory: GABA, glycine - all amino acid NTs
35
PNS neurotransmitters
- excitatory: Ach, adrenaline, NA - inhibitory: NA - all amine NTs
36
difference between amino acid/amine NTs and peptide NTs
- amino acid/amine: made in cytosol of axon terminal and bundled into vesicles + faster transmission - peptides: made in cell body and transported to axon terminals in secretory granules + slower transmission
37
EPSP vs IPSP
- excitatory post synaptic potential: GP that causes depolarisation (closer to threshold) - inhibitory: GP that causes hyperpolarisation (further from threshold) - note: post synaptic neurons can receive input from both EPSPs and IPSPs and then the cell body decides whether the threshold has been reached or not > AP
38
2 types of neurotransmitter receptors
- ionotropic and metabotropic
39
ionotropic receptor
- receptor combined w/ ion channel - ion channel opens when ion (ligand) binds - rapid but short lived transmission
40
metabotropic receptor
- ion channel + separate receptor - NT binding to the receptor triggers a cascade of events (G-proteins) which leads to opening of ion channel - slower response but amplifies response of initial neurotransmitter
41
3 ways the action of a NT is terminated
- taken back up into pre-synaptic neuron - degraded by enzymes - diffuse away from synapse
42
KDR (potassium delayed rectifier) channel
- activated by depolarisation - increases rate of decay of the AP
43
what does the GABA ionotropic receptor conduct?
- Cl- ions
44
nervous tissue embryology
- ectoderm - neural plate forms CNS - neural crest forms PNS