Download MBBS Physiology Presentations 31 Action Potential Lecture Notes

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produced by application of adequate stimulus to
an excitable tissue.

oAction potential = "impulse"

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oChanges during AP ? Depolarization followed
by repolarization of membrane

o Recording of AP in nerve fiber - monophasic

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Recording

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R

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stimulator

CRO

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electrode

+40

V

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e

+20

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pol

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(m 0

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nt -20

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polarization ati

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pot -40

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ne -60

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bra -80

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M

1 msec

Time ( msecs. )

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1 - Stimulus artifact

5

+30

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2 - Latent period
3 - Local potentials

0

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4 - Rapid depolarization

4

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6

5 - Overshoot
6

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Firing

- Rapid repolarization

level

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7 - After depolarization

3

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7

8 - after hyperpolarization

2

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-70 1

8

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Time in msec

Events during A.P. ?
1) Stimulus artifact ? due to leakage of electric

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current from stimulating electrode to recording
electrode

2) Latent period ? It is isoelectric period. Indicates

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the time taken by the impulse to travel from
stim. electrode due to the recording electrode.
Duration varies with the distance between two
electrodes.
3) Local potential ? slow depolarization

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produced due to opening of Na+ channels

Firing level ( threshold potential ) ? membrane
potential at which rapid depolarization begins ?

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which corresponds to 15 mV of depolarization
from RMP.(-55mV )

4)Rapid depolarization ? due opening of fast

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voltage gated Na+ channels which causes entry
of Na+

5) Overshoot ? due to EqNa+ is + 60mV.

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6) Rapid repolarization ? due to closure of voltage

gated Na+ channels and opening of slow voltage
gated K+ channels which increases K+ exit &
stops Na+ entry.

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Afterpotentials ?

7) Afterdepolarization ? reduced rate of
repolarization due to accumulation of K+ on the outer
side of membrane.

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8) Afterhyperpolarization ? due to incomplete closure
of K+ channel causing excess efflux of K+.

Membrane potential comes to resting level by Na+

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-K+ pump.

Ionic basis of A.P.-

I. Local potentials ? partial opening of Na+

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channels influx of Na+ along the electrochemical
gradient causing slow depolarization

At firing level ? rapid opening of activation gates of

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voltage gated Na-channels.

II. Rapid depolarization ? influx of Na+ causes
depolarization which further increases opening of
Na channels (positive feedback mechanism)

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III.Overshoot ? membrane potential becomes
+ve because Eq Na+ is + 60mV
Peak at +30mV ? Na+ entry stops because of
closure (of inactivation gates of ) Na+ channels and
opening of voltage gated K+ - channels

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IV.Rapid repolarization ?increase in K+ efflux
along electrochemical gradient.

V. After potential -

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Va ) After depolarization ?slow repolarization due
to reduced rate of efflux of K+ caused by
accumulation of +ve charge on outer side, RMP is
reached

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Vb )After hyperpolarization ? K-channels remain
open for longer period causing excess efflux of K+
resulting in hyperpolarization

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VI. Hyperpolarization is corrected by Na+-K+ pump
With each AP very small difference in conc.
of Na+ & K+ in ICF & ECF.

Types of AP ?

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1 Spike potential- in nerve and skeletal muscle

2 Plateau potential ? in cardiac muscle

3 Slow potential ? in smooth muscle

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Role of Ca++ in A.P. ?

Ca++ is a membrane stabilizing factor .
Ca++ conc. early opening of voltage

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gated Na+ channels excitability