1-Action Potential Flashcards

1
Q

excitable cells

A

nerve + muscle

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2
Q

types of electrical signals

A
  1. local/passive: receptor potential, synaptic potential
  2. active: action potential (stim in brain)

main difference that active does not decay over distance like passive

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3
Q

circuit of excitable membrane

A

bilayer acts as capacitor to slow the charge/time constant*

*amount of time for voltage to change by 63% of eventual new steady state value

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4
Q

passive conduction

A

-signal at the site of stimulation

-will decay over distance

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5
Q

voltage gated Na channels

A

2 gates: activation + inactivation
3 states: closed (resting), open (activated), inactivated
-always in that order

tetrodotoxin from puffer fish blocks Na channel

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6
Q

voltage gated K channel

A

1 gate
2 states: closed (resting), open (slow activation)

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7
Q

action potential steps

A
  1. resting state- both Na and K channels closed
  2. depolarization- Na channel opens, K stays closed
  3. rising of action potential- Na open, K closed
  4. action potential- peak of voltage, overshoot
  5. falling phase- Na inactivates, K opens, repolarize
  6. undershoot- K stay open prolonged

Na cycle fast regeneration, K cycle slower

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8
Q

membrane permeability during AP

A
  1. resting- K>Na
  2. rising- Na inc
  3. AP- Na>K
  4. falling- Na dec
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9
Q

shape of action potentials

A
  1. cardiac- AP w/ Ca plateau, slower
  2. skeletal muscle- no plateau, sharper peaks
  3. neurons- vary based on type
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10
Q

local anesthesia

A

blocks Na channels to inhibit action potentials and reduce pain

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11
Q

voltage threshold

A

AP’s are all or nothing so indicates a threshold

lowest voltage/minimal depolarization required to drive Na channels into fast feedback loop

above threshold stimulation not needed

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12
Q

factors affecting AP threshold

A
  1. Na channel
  2. K channel
  3. external Ca- indirectly thru Na channels open probability, direct relation to threshold
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13
Q

hypocalcemia symptoms

A
  1. neuropsychiatric
  2. neuromuscular irritability (Chvostek, Trousseau)
  3. cardiovascular
  4. autonomic

bc lower threshold required so more spasms/contractions

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14
Q

Chvostek sign

A

contraction of muscles @ eye, nose, mouth but not very sensitive or specific

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15
Q

Trousseau sign

A

muscle spasm of hand and forearm, more specific and sensitive

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16
Q

hypercalcemia

A

increases threshold so larger amount of depolarization needed to reach threshold

fatigue, muscle weakness, diminished reflexes

17
Q

refractory periods

A

absolute: no response to second stimulus bc Na channels inactivate

relative: second response possible but greater cost, bc K channel prolonged open

set up upper limit of firing frequency and unidirectional propogation

18
Q

AP propagation

A

if axon stimulated in the middle the current flow in both directions so AP goes both directions theoretically

19
Q

unidirectional propagation

A

stimulus at initial segment of axon with lowest threshold to open Na channels then flows down axon

some will flow back upstream but since Na channels inactive nothing happens

20
Q

axon size

A

larger axon diameter = faster axon conducts potential
-electrical conductance inc faster than capacitance

velocity = square root of radius

21
Q

myelination

A

greatly dec axon capacitance (bc capacitors connected in series) and inc membrane resistance = effective insulator

inc action potential conduction speed (saltatory conduction)

22
Q

myelin sheath composition

A

cholesterol
lipids
proteins

23
Q

Nodes of Ranvier

A

where Na channels are located high density so where AP generated, unmyelinated segments

24
Q

saltatory conduction steps

A
  1. AP at one node = current flow to next node
  2. new node reaches threshold = new AP jump to next node

fast bc no time wasted generating nodes in myelin covered and capacitance is lower

energy efficient bc less membrane to generate AP so less Na flows into cell aka less work for pump

length not matter

25
Q

Schwann Cells

A

myelinate a single axon in PNS

26
Q

oligodendrocytes

A

myelinate multiple axons in CNS

27
Q

Multiple Sclerosis

A

demylelination disease of CNS that damages axons

autoimmune attack oligodendrocytes

28
Q

Guillain-Barre Syndrome

A

demyelination of PNS, autoimmune

muscle weakness and paralysis but can recover bc remyelinaton/regeneration

maybe after infection or stomach flu