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Block 3 Up To Quiz 1 > Action Potentials and AP Propagation in Nerves and Cardiac Cells > Flashcards

Action Potentials and AP Propagation in Nerves and Cardiac Cells Flashcards

1
Q

Action potentials are

A

fundamental mechanism for electrical signaling within neurons and muscle cells and between nerves and muscle

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2
Q

what happens once AP generated

A

generated at point A propagated to point B; propagate by combo of passive spread form pt A through low resistance of cytoplasm ot pt B where new AP is generated

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3
Q

why are APs regenerative

A

bc they are all or nothing events that reproduce themselves at diff pets of cell or along axon

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4
Q

what determines direction of AP propagation

A
  • location of initating stimulus

- number of Na+ channels available to be activated in direction current flowing

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5
Q

action potential is what direction in axons of nerve

A

unidirectional in axons of nerve from pt of initiation in axon hillock -> presynaptic terminal bc inactivation Na+ channels at initiation point means although current spreads all direction next action potential generated must be in unexcited axon closer to nerve terminal

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6
Q

cardiac muscle action potential

A

action potential propagated from excited cell to unexcited cell via gap junctions that connect them (wnt go to previously excited cell bc it is refractory)

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7
Q

myelination of axons in Schwann cells

A

optimizes cytoplasmic current flow and increases speed and safety factor for conduction

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8
Q

action potentials of different cell types

A

are different in shape and duration bc cells contain different variants of voltage-sensitive ion channels that participate in generating their action potentials
- cardiac myocytle action potential MUCH longer (500x) than action potential of neuron; neuronal signaling is v fast

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9
Q

SA node cells

A

Sino-atrial node cells are pacemaker for cardiac cycle

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10
Q

depolarizing phase of action potential of SA node cells

A

due to opening of L-type voltage-gated calcium channels

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11
Q

SA node cells voltage-gated Na+ channels

A

do not express voltage gated Na+ channels

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12
Q

SA node action potentials

A

initiated by opening of 3 types voltage-gated channels and repolarization is due to activation of single type voltage-gated K+ channel in delayed rectifier group

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13
Q

SA node input

A

SA node generates action potentials w/o external stimuli; SA nodes reach AP threshold via mechanism intrinsic to SA cells

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14
Q

Why are SA node cells pacemaker cells

A

bc SA node cells have set of channels that produces funny current If
- these channels = hyperpolarization and cyclic-AMP activated cation channels aka HCN channels

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15
Q

HCN channles

A

aka hyper polarization and cyclic-AMP activated cation channels
characteristics:
1. Activated by hyperpolarization and inactivated by depolarization
2. Activation is modulated by increasing or decreasing intracellular cAMP concentration
3. Permeable to Na+ and K+ but more permeable to Na+ ions so equilibrium potential is about -30mV

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16
Q

cAMP

A

cyclic nucleotide produced from ATP by adenylate cyclase

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17
Q

SA node cells resting membrane potential

A
  • don’t truly have one bc int contain voltage insensitive K+ channels
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18
Q

HCN channel inactivation

A

inactivate well before peak of AP depolarization; do not interfere with repolarization occurring after delayed rectifier channels activated; HCN channels reopen during down stroke of AP bc open probability continues to increase during repolarization phase culminating in gradual depolarization (pacemaker potential) which brings cell membrane closer to AP threshold

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19
Q

SA activation

A

HCN channels open and depolarize SA node cells, fit opening voltage-gated transient (T-type) Ca2+ channels activate these two things together -> depolarization SA node cells enough to activate L-type Ca2+ channels which responsible for upstroke SA node action potential -> cell depolarizes to >-20mV voltage-gated delay rectifier type K+ channels open and action potential begins to depolarize

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20
Q

T type channels

A

transient bc activate and inactivate like voltage gated Na+ channels in other excitable cells

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21
Q

control of pacemaker rate

A 
controlled by ANS
symp input (norepinephrine and epinephrine) -> increase pacemaker rate
parasympathetic input (acetylcholine via muscarinic receptors) -> slows action potential
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22
Q

Sympathetic input pacemaker

A
  • B adrenergic effects symp stimulation -> increase in intracellular cAMP -> activation HCN channels and increase slope pacemaker potential
  • increase cAMP -> increase L-type Ca2+ channel phosphorylation potentiates increases open time of channels and permits increase in calcium influx
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23
Q

parasympathetic input pacemaker

A

slows heart rate
- produced by acetylcholine release from vagus nerve and subsequent activation of cardiac muscarinic receptors; intracellular effect is decrease production cAMP -> prolonged hyperpolarization and decrease of slop of pacemaker potential

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24
Q

action potentials in ventricular myocytes are long because

A

upstroke of ventricular mycocyte AP mediated by opening fast-activating Na+ channels and depolarization is sustained by activation of L-type Ca2+ channels which are main component responsible for long plateau

  • voltage and time dependent activation L-type Ca2+ channels is highly regulated by synaptic and hormonal stimulation
  • ventricular myocyte action potential depolarization turns off cardiac inward rectifier currents
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25
Q

ventricular myocyte action potential depolarization turns off cardiac inward rectifier currents

A

occurs because large intracellular cations
- channel blockade -> depolarization maintained and Ca2+ entry through L-type channels sustained allowing intracellular Ca2+ concentration to rise sufficiently to activate ryanodine receptors to stimulate cardiac muscle contraction if these channels were blocked K+ efflux would oppose activation Na+ and Ca2+ channels and cell would depolarize too rapidly and cardiac muscle would not contract

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26
Q

repolarization cardiac myocyte

A
  • cardiac version delayed rectifier K+ channels (Ikv1.5) activate slowly compared to Ikv1 types in neurons
  • this allows appreciable K+ efflux doesnt begin till after Ca2+ dependent plateau developes, longer plateau means more time for Ca2+ to enter to ensure muscle contraction
  • slow Ikv1.5 return membrane toward resting potential inward rectifier K+ channels responsible for resting potential in cardiac myocytes become unblocked bc forces driving Mg2+ and polyamides from cytoplasm into channels are reduced -> hand over of repolarization mechanisms from Ik1.5 to Ik1r channels
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27
Q

for action potential to participate in signaling

A

action potentials generated at point A capable of changing membrane potential nearby and generating new action potential in previously unexcited patch membrane downstream

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28
Q

propagation of action potential from one compartment to another requires

A
  1. A driving force for current flow

2. A connection between two compartment

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29
Q

Driving force

A

difference in membrane potential (transmembrane voltage) btwn compartment that generated AP and compartment that hasn’t yet generated AP

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30
Q

current flow between excited and adjacent resting patch of membrane

A

passive; if passive current spread from upstream depolarization is sufficient to activate more than a few voltage-gated ion channels in downstream patch excitable membrane than AP generated

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31
Q

propagation of action potential at ummyelinated axon

A

T1 point A: depolarizing stimulus -> activation voltage gated Na+ channels -> Na+ flows into axon -> depolarizes membrane -> activates more Na+ channels -> threshold reached -> action potential ->
T2 point B: curent flows through cytoplasm to point B-> new action potential generated
T2 point A: voltage-gated K+ channels open slowly starting at T1 open at T2 -> K+ efflux -> repolarizing membrane
This process continues down axon action potential to next point repolarization at previous pt where just had last AP

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32
Q

To initiate an AP

A

-stimulus must activate many Na+ channels so pos feedback from small depolarization gained from addition newly activated channels

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33
Q

AP threshold

A
  • membrane potential where majority of available Na+ channels open and membrane potential rises rapidly during upstroke of AP
  • “membrane potential where no additional external stimulation needed for AP to fire (ie intimate and continue the upstroke)
  • Threshold carries based on type of cell, diff ionic conditions,
  • ability of patch of nerve to generate an AP dependent on density of voltage gated Na+ channels in unexcited patch that are available
34
Q

Action potential vs spread of current

A
  • action potential propagation is unidirectional along axon while passive spread of current in axoplasm is in both directions; this is bc Na+ channel inactivation keeps action potential propagation unidirectional
35
Q

action potential propagation inclues

A

both ionic currents through open channels and passive currents associated with charging and discharging membrane capacitor

36
Q

capacitative current

A

change in charge on phospholipids

37
Q

Na+ and K+ action potential

A

K+ and Na+ channels open Na+ flows into K+ flows out of axon/ cell Na+ channels then in refractory period and temporarily inactivated and K+ efflux through open channels depolarizes membrane

38
Q

contributions to refractoriness of axon upstream of AP

A
  • gK+ remains high are action potential and Na+ channels are inactivated -> refractoriness axon upstream of AP
39
Q

propagation of action potential

A

Na+ entry through open Na+ channel -> difference in membrane potential between open depolarized channel and adjacent membrane at resting potential -> positive charge from L to R building in cell -> positive charge on extracellular side of membrane moving away from cell membrane back toward L side patch where extracellular potential more negative -> continued movement pos charge in cytoplasm L to R depolarizes membrane potential past threshold Na+ channel opens -> Na+ enters cell -> new action potential -> depolarize next patch membrane to R

40
Q

myelinated nerve fibers

A
  • In CNS oligodendrocyte glial cells ensheath axons
  • in PNS myelination by Schwann cells wrapped around axons
  • propagation action potential same as in unmyelinated Neve fiber but excitable membrane patches containing voltage-gated Na+ channels located at nodes Ranvier while membrane sheathed in myelin inexcitable
41
Q

speed action potential propagation determined by

A
  • resistance cytoplams

- resistance of pathway across membrane

42
Q

myelin and transmembrane current

A
  • multiple layers of myelin create high resistance barrier between cytoplasm and extracellular space preventing transmembrane current leaking across cell membrane
  • bc v little current leaking action potentials propagate faster in myelinated axons than unmyelinated axons
43
Q

action potential propagation in myelinated nerves called

A

saltatory conduction (means to jump)

44
Q

action poteital propigation in myelinated nerves

A
  • same steps as in unmmyelinated but voltage gated Na+ channels at nodes ranvier rest of membrane inexcitable
  • axon membrane capacitance reduced and axon membrane resistance increased in myelinated axon which allows for more efficient flow current to next node through low resistance of cytoplasm
45
Q

demyelination nerve fibers

A

autoimmune dx and other demyelinating disorders myelin sheath damged by inflammation and may be lost permanetely

  • acutely demyelinated axon segments btwn nodes Ranvier int express Na+ channels and depolarization at one node must be lrg enough to reach next node w/o insulation
  • acute demyelination (loss myelin patchy) -> action potential conducted more slowly
  • loss myelin involving more than few nodes can -> compete failure of propagation
  • as more myelin lost -> loss protein secreted by Schwann cells (caspr) and Na+ and Kvr channels become more evenly distributed along length axon allowing some restoration of conduction (this recovery will take time and will only be partial)
46
Q

demyelination worse than not being myelinated at all

A

bc cell membranes of unmyelinated nerve fibers lack high resistance insulation which makes them more prone to leakage but excitable membrane patches in these cells contiguous with one another and leak of current between two patches of excitable membrane = v compensated for by leg influx depolarizing current provided and voltage gated Na+ and K+ channels which are uniformly distributed and close enough together to allow for effective action potential propagation

47
Q

explain slow conduction bc demyelination

A

depolarizing current generated by Na+ influx in L node escapes across demyelinated segment of fiber rather than flowing through axoplasm so membrane R node less depolarized and it takes longer for sufficient depolarization to accumulate in R node and for it to reach threshold and fire

48
Q

propagation cardiac action potentials

A
  • propagation action potentials between cardiac myocytes necessary to synchronize cardiac contraction
  • rapid AP propagation heart possible bc low resistance pathways formed by open gap jnxions electrically coupling cardiac cells to each other longitudinally and transversely -> synchronized network referred to as syncytium
49
Q

gap junctions between cardiac cells

A

comprised of connexons which are couplings of 6 connexins that terminate regions of cell membrane in cardiac cells

50
Q

propagation action potential in cardiac cells

A

occurs bc depolarizing current generated by excited patch membrane in one myocyte transferred via connexon to unexcited patch membrane in adjacent myocyte

51
Q

myocytes in cardiac cells separated by

A 
gap junctions (electrically) (actual membrane patches are contiguous within given cardiac muscle cell)
- gap junctions provide conduit for current flow from excited to unexcited myocyte
52
Q

propagation of action potential between cardiac cells occurs bc

A

depolarizing current generated by excited patch membrane in one myocyte transferred via connexon to unexcited patch of membrane in adjacent myocyte

53
Q

resistance between adjacent cells in normal heart

A

very low because gap junctions between myocytes nearly all open

54
Q

nerve and muscle cell different action potentails

A

different shapes and speeds result of different ion channels expressed by diff types excitable cells

55
Q

what plays most critical role in propagating action potential in nerves

A

voltage-dependent activation and inactivation of Na+ channels

56
Q

addition of depolarizing current to interior oc cell

A

stimulates opening of voltage-gated Na+ channels causing capacitance across membrane patch to discharge -> rapid change charge depolarizing membrane above threshold potential for opening nearby fast sodium channels

57
Q

Na+ influx via open Na+ channels

A

creates voltage gradient between excited region membrane and neighboring unexcited regions; flow depolarizing current from excited to unexcited region raises unexcited to threshold potential and opens Na+ channels

58
Q

flow of action potential along axon

A

hillock -> terminal

59
Q

axon terminal voltage gated ion channels

A

no voltage gated Na+ channels yes voltage gated Ca2+ channels, let Ca2+ in allow vesicle fusion and leading to neurotransmitter release

60
Q

what propagates action potential

A

phospholipid bilayer cell has neg charge and when Na+ ions cross -> change membrane charge when crossing bc change voltage in cell -> change charge membrane and the disrarche of charges of membrane propigates action potential

61
Q

large vs small diameter axons

A

large diameter axons conduct faster than small bc resistance to current flow through cytoplasm decreases as cross sectional area axon increases

  • small usually carry pain and temp
  • large usually carry light tough
62
Q

if you bang eblow

A

starting in middle long axon so action potential can go both ways at first bc pt toward hand hands been activated leads to stinging down arm ect.

63
Q

refractory region

A

in temporary condition reverts back to available when membrane repolarizes

64
Q

membrane capacitance discharge

A

allows current flow to be fast

65
Q

Nodes of ranvier

A

have K+ channels caspr Na+ channels caspr K+ channels

66
Q

stages SA node AP

A

if -> ica(t) -> ica(l) -> ik -> if

67
Q

cardiac myocyte stages AP

A

ik -> ina -> ikto -> Ica(l) ->ik

68
Q

what are necissary for pacemaker function

A

HCN channel properties required for pacemaker function

69
Q

HCN channels and Na+

A

HCN channels let Na+ through BUT are not Na+ gated channels (which are fast voltage gated)

70
Q

SA node pacemaker potentials

A
  1. HCN channels (If) open Na+ influx depolarizing membrane
    2a. Transient Ca2+ (T-type) channels rapidly open and depolarize SA node above action potential thrshold
    2b. HCN channels turn off when membrane depolarized
    3a. Depolarization activates L-type Ca2+ channels generating upstroke action potential
    3b. Transient Ca2+ (T type) channels turn off
    4a. Voltage activated K+ channels open and depolarize membrane
    4b. Repolarization situations activation HCN channels cycle repeats
71
Q

ikto

A

in cardiac mycocute AP; transiet k+ current brief and all it does is stop AP from being > amplified than it is an irregularity in this current -> change current

72
Q

when do voltage gated Ca2+ shut in cardiac myocyte AP

A

when K+ shuts them down

73
Q

action potential through heart

A

SA node action potential rapidly conducted through atrium to AV node through His-purkinje network to ventricular myocardium

74
Q

pore structure of gap junction channel

A

a lot of negatively charged Has lining core allows for cations to flow through

75
Q

excitable cells have large

A

resting membrane potential that facilitates recovery voltage gated Na+ and Ca2+ from inactivated states

76
Q

what excitable cells do not have all or none action potentials in response ot extrinsic stimuli

A

pacemaker cells

77
Q

pacemaker cells do not have

A

RMP

78
Q

what provides intrinsic depolarizing effect in pacemaker cells

A

HCN channels

79
Q

changes in serum chemistry can lead ot

A

changes in electrical activity; low Ca2+ levels usually bc kidney issue

80
Q

purpose of neuron

A

gather incoming signals, integrate them and transmit info to connected cells w/ in network by propagating action potential

81
Q

action potentials conduction between cardiac cells through

A

gap junctions

Block 3 Up To Quiz 1 (24 decks)

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