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Basic Principles Of Medicine 1-FTM 1 > Action Potentials > Flashcards

Action Potentials Flashcards

1
Q

What is an action potential?

A

A transient, rapid depolarization of the membrane potential

Critical for communication (neurons) and as action trigger (myocytes, endocrine)

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2
Q

Summarizes what causes the action potential

A

Due to swing of Vm from Ek to Ena and back to Ek
-in cardiac pacemaker cells, calcium channels are also important, with Ca2+ ion influx playing the same depolarizing role as Na+ion influx

  • membrane fractional conductance
    • high for K+ at rest
    • high for Na+ only during depolarizing phase of the AP
    • due to voltage-gated Na+ and K+ channels
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3
Q

List the functional phases of AP

A
  1. Rest membrane potential
  2. Graded depolarization phase
  3. Rapid depolarization phase
  4. Repolarization phase
  5. After hyper polarization phase
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4
Q

Explain the stages of the action potential

A
  1. Positive charges flow into the cell and causes a slight depolarization
  2. Threshold is reached. Voltage-gated Na+ channels begin to open fully, leading to more positive charge entering cell and further depolarization
  3. Rapid depolarization as the Na+ conductance increases dramatically and the membrane potential approaches the equilibrium potential for Na+
  4. Peak AP. Na+ channels are fully open and Na+ conductance has peaked as Vm approaches ENa
  5. Na+ channels begin to inactivate and Na+ conductanceak drops at the same time as the K+ conductance starts to develop. Vm peaks and starts to swing back towards Ek
  6. Refractory period. Since K+ channels are open and Na+ channels are in their inactive state, Vm gets close to Ek, below the resting membrane potential. Due to closed inactivation gates Na+ channels are blocked, no further APs can be conducted.
  7. The channels reset to their normal resting conditions, resting membrane potential is restored. All Na+ channels are now out of their inactive state and can be reactivated to form another full action potential
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5
Q

What is channel gating?

A

Opening and closing of the channel (gating)- regulated by the electric field, ligands, calcium, phosphatase/kinase activity, cAMP, oxygen carbon dioxide, etc.

Gates exist in closed or popes states, transitions are rapid. There may be more than one gate in a channel

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6
Q

What direction is flow determined in channel gating?

A

In some channels flow can occur in either direction (non-rectified), some channels show uni-direction flow

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7
Q

What determines open probability in channel gating ?

A

The time a channel spends in the open state determines its open probability (Po)

More ion-specific channels in the membrane = higher conductance for that ion

Each channel has a single unit conductance, I.e. a per channel conductance

Total conductance = number of channels * unit conductance *open probability

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8
Q

What are gates?

A

Barriers to ion flux

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9
Q

What are the 2 gates to Na+ gates?

A

Activation gate (m), Extracellular

Inactivation gate(h), intracellular

Each gate can block channel independently

The combined action of both gates provides the transient high Na+ conductance that carries the AP

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10
Q

How is voltage gating done in the Nac gate?

A
  • depolarization above threshold ( about -50 mV) opens activation gate
  • inactivation gate closes after slight delay at peak of AP
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11
Q

Explain the inactivation gate time delay

A
  • gates have different rates of operation
  • m gate is quicker than h gate
  • on depolarization the inactivation gates lag behind the activation gate
  • hence both gates are open only for a brief period
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12
Q

Describe the Nav gate during the resting phases

A

Resting state

Activation gate closed and inactivation gate open

-no flux of Na+

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13
Q

Describe the Nav gate during the depolarization phase

A
  • activation gate open and inactivation gate open

- channel open, full Na+ flux

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14
Q

Describe the Nav gate during the repolarization phase

A
  • activation gate open but inactivation gate closed
  • no flux of Na+
  • channel cannot be activated at this time- -absolute refractory period.
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15
Q

Describe the Nav gate during the reset to resting state

A
  • activation gate closes whilst inactivation gate opens

- once reset the absolute refractory period is over

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16
Q

Contrast the refractory periods.

A

Absolute refractory period
- during repolarization phase when inactivation gates are closed

-no new AP can be initiated or conducted because Nav channels are blocked

Relative refractory period
-after absolute refractory period during after hyper polarization phase

  • starts when the Nav inactivation gates are open again
  • APs initiation is inhibited due to after hyper polarization (increased K+ conductance)
  • but principally APs can again be initiated since Nav channels have reset(inactivation gates open)
17
Q

K+ channels are also voltage sensitive…

A

Hence potassium conductance is increased by depolarization

  • time and voltage dependent activation of K+ channels
  • slow time activation compared to Na+ channels allows AP to peak before onset of K+ current
  • Delayed rectifying K+ channel
18
Q

Explain the physiological impact of rectification

A
  • delayed rectifier K+ channels (family of different channels)
  • voltage and time dependent activation of K+ conductance
  • highly expressed in neurons
  • role is to reset Vm towards Ek by increasing fractional K+ conductance
  • inward rectifying CK+ channels (Kir)
  • voltage but not time dependent
  • current rectification (one-way flow)
  • inwards rectifying K+ channels have strong preference for inward K+flux
  • expressed in heart and vasculature
19
Q

What is the effect of hypocalcemia?

A

Threshold is lower, closer to RMP —> increased excitability. Can lead to tetany (increased muscle tone)

20
Q

What is the effect of hypercalcemia?

A

Threshold is further from RMP —> decreased electrical excitability. May lead to weakness, but uncommon

21
Q

What are the effects of slow depolarization ?

A
  • sodium channel inactivation gates close in a fraction of the channel population prior to depolarization threshold being reached
  • a fraction of the sodium channels become refractory
  • delayed rectifier K channels open and increase basal K+ conductance, stabilizing the membrane potential close to Ek
22
Q

What are the effects of long slow depolarization?

A
  • tends to lock inactivation gates closed on Nav like in absolute refractory period
  • Tends to increase delayed rectifier K channel conductance
  • Both tend to reduce electrical excitability
  • Means rate of depolarization determines the likelihood of action potential firing
  • Clinically relevant with changes in plasma (K+)
  • Leads to weakness and paralysis in worst case
23
Q

What is the depolarizing pre-pulse?

A

Stimulus to threshold stimulates an AP

Sub-threshold stimulus= no AP

Pre-sub threshold stimuli- close h gates of the Na channel and the resulting AP only has a fraction of the total channel population to stimulate - so the AP is smaller and sluggish

24
Q

What is the clinical significance of hyperkalemia?

A

Normal range [K+] 3.5 to 5.0 mmol/l

Hyperkalemia means increased extracellular [K+]

Nernst- depolarization of Ek

  • a fraction of Na+ channels open and close but never reset
    • a permanent refractory period, channel inoperable

-K+ conductance increases and stabilizes membrane potential close to Ek

25
Q

What are the consequences of hyperkalemia?

A
  • membrane is at a stable, slightly depolarized state with fewer active Na channels
  • action potentials are sluggish or absent
  • weakness of paralysis
26
Q

Explain detail the effect and cause of hypokalemia

A

Decreased extracellular [K+]

Nernst-hyper polarization of Ek

-consequences at first thought: membrane is at resting potential that is more negative and thus further away from AP threshold. Depolarizing stimuli should have to be much greater to generate an AP, resulting in lower excitability

27
Q

In hypokalemia, why is the AP Is also decreased?

A
  • Lower RMP —> less background Na+ channel opening and closing
  • hence more Na+ channels are ready to response to depolarizing stimuli
  • More K+ channels are closed, hence less opposing force to depolarization
28
Q

What are the electrochemical effects for hypokalemia ?

A
  • steeper slope of depolarization (excitability) and lower threshold potential for full depolarization
  • Na-K ATPase also reduced since [K+] in ECF is reduced
  • the resulting intracellular [Na+] increase inhibits the efficacy of the Na+/Ca+ anti porter, the main mechanism to reduce intracellular [Ca2+]
  • hence intracellular [Ca2+] remains elevated after action potentials
29
Q

What are the consequences of hypokalemia?

A

Muscle weakness, cramps, spasms, respiratory swallowing or failure, cardiac arythmia, paralysis

30
Q

What are the non-clinical consequences of changes in sodium?

A

Serum [Na+] has little effect on RMP as the fractional sodium conductance at rest is minimal

But it does change the rate of sodium influx
-reducing [Na+] results in slow influx and smaller, sluggish APs

31
Q

What are the clinical consequences of changes in sodium?

A
  • little effect on AP
  • significant effects on cell volume
  • hyponatremia most likely related to kidney function

Basic Principles Of Medicine 1-FTM 1 (39 decks)

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