ionic basis of AP Flashcards

1
Q

whats a AP

A

= Rapid and transient change in voltage across the membrane
- Depends on ionic gradients & relative permeability of the membrane
- Generated in excitable cells in response to pre-synaptically released neurotransmitter
- All or nothing (threshold level)
- Propagated over long distances without loss of amplitude

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2
Q

draw AP

A
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3
Q

APs in different tissues: axon

A

RMP: -70
peak: +30
duration: 0.5ms

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4
Q

APs in different tissue: skeleteal muscle

A

RMP: -90
peak: +40
duration: 0.5 ms

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5
Q

APs in different tissue: sino-arterial node

A

RMP: -60
peak: +30
duration: 100ms

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6
Q

APs in different tissue:

A

RMP: -90
peak: +30
duration: 100ms

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7
Q

what causes rapid depolarization of the cell membrane

A

The sodium hypothesis
- Because (Na)0 > (Na)I -> depolarization involves a rapid & highly specific increase in the permeability of the membrane for Na+ ions
 Resulting membrane potential approaches Ena

  • Discrepancy
  • Trajectory of an AP is limited by the Ena and EK
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8
Q

what channels mediate the repolarization phase

A

K+ channels

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9
Q

controlling channel activity possibilities

A
  1. Ligand gating
    - Channel opens or closes in response to the binding of a chemical ligand
  2. Voltage gating
    - Opens or closes in response to changes in membrane potential
  3. Mechanical gating
    - Channel open or closes in response
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10
Q

pharmacological inhibition of Na+ and K+ channels

A

TTX= Na+ (VT) channel blocker
-> Na influx is delayed
TEA= K+ (VT) channel blocker
-> K+ eflux delayed
- Inwards & outwards currents are mediated by voltage-gated Na+ and K+ channels, respectively

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11
Q

membrane repolarization

A

= Na+ (VG) channel inactivation & delayed K+ (VG) activation
- na (VG) channels close due to inactivation
-> K+ (VG) channels open

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12
Q

why is it important for K+ (VG) channels to open with delay

A
  1. Allows for Depolarization and Action Potential Peak
    - If K⁺ channels opened simultaneously with Na⁺ channels, the outflow of K⁺ would counteract the inflow of Na⁺, making it harder to depolarize the cell membrane to the AP threshold or peak. The delay in K⁺ channel opening allows the Na⁺ influx to occur first, ensuring a strong and rapid depolarization.
  2. Helps Control the Repolarisation Phase
    - The timing of K⁺ channel opening is critical because it helps end the AP in a controlled manner, restoring the membrane potential back to a more negative resting state.
  3. Prevents Premature Hyperpolarization
    - The delay ensures that K⁺ channels open only after the AP has peaked, facilitating a smooth return to resting potential without premature inhibitory effects.
  4. Ensures Refractory Period and Directional Propagation
    - The delayed K⁺ outflow contributes to the refractory period, a phase during which the neuron cannot immediately fire another AP. This refractory period helps in resetting the ion channels and preventing backflow, ensuring that the AP travels in one direction along the axon.
    - Without the delay in K⁺ channel opening, the timing of the refractory period would be altered, potentially leading to uncoordinated signaling or back-propagation of APs.
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13
Q

time course of conductance changes during AP

A

-> - No K+(VG) channels (or TEA) -> longer AP = no afterhyperpolarization (AHP)

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14
Q

what causes undershot after hyperpolarization

A
  1. Delayed Closing of Voltage-Gated K⁺ Channels
    - During repolarization, K⁺ channels open to allow K⁺ ions to flow out of the neuron-> drives the membrane potential back toward a negative value. However, these channels do not close immediately once the membrane reaches its resting potential.
    - Voltage-gated K⁺ channels slowly close- K⁺ continues to exit the cell for a short period even after reaching the RMP -> MP dips slightly below the usual RMP
  2. Increased K⁺ Conductance Compared to Resting Conditions
    - During the after-hyperpolarization, the membrane has a higher K⁺ conductance than at rest because some of the voltage-gated K⁺ channels are still open.
    - This enhanced K⁺ permeability pulls the membrane potential closer to the K⁺ equilibrium potential, which is more negative than the resting potential, causing a temporary hyperpolarization below the resting level.
  3. Leak channels
    - The leak channels and Na⁺/K⁺ pump help restore the ion distribution and return the membrane to the typical resting potential.
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15
Q

consequences of undershot after hyperpolarization

A

-> Increase the Refractory Period: By making the membrane more negative than usual, it makes it harder for the neuron to fire another AP immediately, enforcing the refractory period and preventing rapid, uncontrolled firing.
-> Regulate Excitability: After-hyperpolarization temporarily reduces neuronal excitability, preventing excessive firing and allowing the neuron to “reset” before the next AP.

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16
Q

what happesn during depolarization

A

Stimulus -> depolarization to threshold -> Na+ channels open -> Na+ enters the cell -> membrane depolarizes

->This positive feedback is the basis of the all or none characteristic of AP

17
Q

diagram of what happens during repolarization

A
18
Q

whats the absolute refractory period

A
  • Na+ channels refractory to any stimulus
  • Short-lasting
  • Na+ channels: open -> inactive
  • K+ channels: closed -> open

-> during de and Repolarizationn

19
Q

What is the relative refractory period

A
  • Na+ channels: inactive -> close
  • Na+ channels need strong (supra-threshold) stimulus to open
  • Can be long-lasting
  • K+ channels: open

-> during after hyperpolarization

20
Q

why absolute and relative refractory periods

A
  • Ensures normal firing rate (e.g., heart rhythm)
  • Maintains unidirectional AP propagation
21
Q

how many ions need to flwo to generate an AP

A
22
Q

local anaesthetics

A

Cocaine: first local anaesthetic (synthetics: procaine, lidocaine)
- They disrupt ion channel function by binding temporarily to the cytoplasmic side of voltage gates Na+ channels
- This results in decreases Na+ entry during AP upstroke