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Anatomy 403 > Changes in Membrane Potential > Flashcards

Changes in Membrane Potential Flashcards

1
Q

electrically excitable

A
  • nerve and muscle cells are specialized to use rapid changes in their electrical properties for signaling or mechanical work
  • due to presence of gated ion channels
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2
Q

dendrites

A
  • numerous
  • receive input
  • generate local potentials
  • LGIC (can also be mechano-gated)
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3
Q

cell body

A
  • integrates local potentials
  • contains cell body and organelles
  • LGIC
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4
Q

axon hillock

A
  • site of AP generation
  • VG Na+
  • VG K+
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5
Q

axon

A
  • send information one way via action potential
  • one per neuron
  • VG Na+
  • VG K+
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6
Q

axon terminal

A
  • release of neurotransmitter
  • VG Na+
  • VG K+
  • VG Ca+2
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7
Q

ligand receptor

A
  1. neuron stimulated by chemical
  2. ion channel opens
  3. ionic current flow
  4. local change in membrane potential
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8
Q

depolarizing

A

toward zero

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9
Q

overshoot

A

polarity reversed (inside positive, outside negative)

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10
Q

repolarizing

A

towards resting membrane potential

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11
Q

resting membrane potential

A

-70 mV

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12
Q

hyperpolarizing

A

more negative than resting membrane potential

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13
Q

types of potentials

A
  • local (graded) potential

- action potential

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14
Q

local (graded) potential

A

small change in membrane potential confined to small region of membrane

  • small distance signals
  • produced by non-voltage gated channels
  • primary at dendrites and cell body
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15
Q

local potential use:

A
  • LGIC (nerve / muscle)

- mechano (sensory receptors)

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16
Q

local potential characteristics

A
  • “graded”
  • decremental
  • depolarizing or hyperpolarizing
  • can summate
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17
Q

“graded”

A

proportional to size of stimulus

  • magnitude of potential can vary
  • strong stimulus = more channels will open
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18
Q

decremental

A

decay with distance from stimulus because charge leaks through membrane
- flow of charge decreases as the distance from the site of the potential increases

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19
Q

characteristic: depolarizing

A

Na+ in

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20
Q

characteristic: hyperpolarizing

A

Cl- in, inside is more positive or K+ out, inside is more negative

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21
Q

summate

A

add together

- if threshold is reached (-55mV) neuron will generate action potential

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22
Q

excitatory

A

depolarizing

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23
Q

inhibitory

A

hyperpolarizng

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24
Q

action potential

A

large and rapid change in membrane potential that propagates over long distances

  • use voltage gated channels
  • only excitable membranes (nerve, muscle cells)
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25
Q

action potential characteristics

A
  • all or none
  • not graded by stimulus size
  • not decremental (self-propagating)
  • cannot summate (refectory period)
26
Q

action potential step #1

A

steady state RMP P k > P Na due to leak channels

27
Q

action potential step #2

A

threshold reached due to local potentials

28
Q

action potential step #3

A

VG Na+ channels open rapidly depolarizing membrane –> Na+ in (positive feedback
- depolarization

29
Q

action potential step #4

A

inactivation of Na+ channels and delayed opening of K+ channels stop depolarization

30
Q

action potential step #5

A

open VG K+ channels depolarize to negative potential (K+ out)
- repolarization

31
Q

action potential step #6

A

slow closing K+ channels hyperpolarize membrane closer to EKj Na+ channels return to closed state
- hyperpolarization

32
Q

action potential step #7

A

Na+ / K+ ATPase establishes RMP

33
Q

local anesthetics (novocaine, lidocaine)

A
  • VG Na+ channel blockers
  • pain receptors can’t send signals to brain
  • NO action potential
34
Q

tetrodotoxin (TTX)

A

VG Na+ channel blocker

35
Q

saxitoxin

A
  • produced by algae

- VG Na+ channel blocker

36
Q

scorpion toxin mechanism of action

A
  • prevents Na+ channel in activation

- blocks neural transmission

37
Q

tetraethylammonium (TEA) mechanism of action

A

blocks VG K+ channels

38
Q

absolute refractory period

A
  • no amount of stimulation will produce another action potential
  • because Na+ channels already open or inactivated
39
Q

relative refractory period

A
  • only a very strong stimulus will produce another action potential
  • hyperpolarization because K+ channels open drives Vm more negative
40
Q

refractory period

A
  • contributes to the separation of action potentials so that individual electrical signals pass down axon
  • as V, approaches RMP, threshold stimulus strength decreases
41
Q

propagation

A

one produces the next

42
Q

unmyelinated fibers

A
  • local current from the opening of LGIC in dendrites and cell body causes an action potential to be insulated in region 1
  • local current depolarizes in region 2
  • will not propate backwards because of refractory period
  • region 1 is refractory (Na+ channels inactive) –> repolarizing
  • ex: digestive system
43
Q

myelination

A

protein and lipid (80%) insulation

44
Q

PNS myelination

A

Schwann cells

45
Q

CNS myelination

A

oligodendrocytes

46
Q

nodes of ranvier

A

not a continuous sheet of insulation in the central nervous system (CNS)

47
Q

myelinated fibers

A
  • VG Na+ channels concentrated at nodes
  • current flows thru axon to next node
  • action potentials ‘jump’ from node to node
  • Na+ ions can’t flow in/out where there is myelin
  • ex: pain receptors
48
Q

conduction velocity increases with:

A
  • axon diameter

- myelination

49
Q

Cm

A

membrane capacitance, electrostatic forces acting through bilayer

50
Q

Rm

A

membrane resistance

- how many leak channels are open

51
Q

Ri

A

current path provided in axoplasm

52
Q

length

A

how far current will flow

53
Q

time

A

time to change Vm

- T is proportional to Cm

54
Q

larger axons

A
  • more cross sectional area
  • more charge carriers
    • leads to lower Ri
  • local current decay less over a given distance
  • larger local current
  • increases conduction velocity
55
Q

internal regions

A

where there is myelin

56
Q

saltatory conduction

A

larger local currents are available to depolarize axon form node to node

57
Q

myelin covering

A

no flow of ions

58
Q

pathogenesis

A
  • increased B and T cell sin CNS
  • increased astrocyte and microglia activity
  • inflammation
  • demyelination and neurotoxicity in CNS
  • current is lost through exposed membrane –> conduction block may occur
  • myelin replaced with scar tissue due to increased astrocyte activity = sclerosis
59
Q

conduction block in MS

A

disrupts ability of neurons to communicate

60
Q

symptoms of MS

A

life expectancy: 5-10 years less than unaffected

Anatomy 403 (13 decks)

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