Download MBBS Physiology Presentations 31 Action Potential Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st Year, 2nd Year, 3rd Year and Final year Physiology 31 Action Potential PPT-Powerpoint Presentations and lecture notes

Action potential

o Action potentials are brief, rapid, large,
propogatory changes in membrane potentials
produced by application of adequate stimulus to
an excitable tissue.

oAction potential = "impulse"

oChanges during AP ? Depolarization followed
by repolarization of membrane

o Recording of AP in nerve fiber - monophasic

Recording

)

R

stimulator

CRO

electrode

+40

V

e

+20

pol

i
a
l
(m 0

ari

e
nt -20

z

polarization ati

pot -40

De

on

ne -60



bra -80

e
m
M

1 msec

Time ( msecs. )
1 - Stimulus artifact

5

+30

2 - Latent period
3 - Local potentials

0

4 - Rapid depolarization

4

6

5 - Overshoot
6

Firing

- Rapid repolarization

level

7 - After depolarization

3

7

8 - after hyperpolarization

2

-70 1

8

Time in msec

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

current from stimulating electrode to recording
electrode

2) Latent period ? It is isoelectric period. Indicates

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

produced due to opening of Na+ channels

Firing level ( threshold potential ) ? membrane
potential at which rapid depolarization begins ?
which corresponds to 15 mV of depolarization
from RMP.(-55mV )

4)Rapid depolarization ? due opening of fast

voltage gated Na+ channels which causes entry
of Na+

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

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.
Afterpotentials ?

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

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

Membrane potential comes to resting level by Na+
-K+ pump.

Ionic basis of A.P.-

I. Local potentials ? partial opening of Na+
channels influx of Na+ along the electrochemical
gradient causing slow depolarization

At firing level ? rapid opening of activation gates of

voltage gated Na-channels.

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

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

V. After potential -

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

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

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 ?
1 Spike potential- in nerve and skeletal muscle

2 Plateau potential ? in cardiac muscle

3 Slow potential ? in smooth muscle

Role of Ca++ in A.P. ?

Ca++ is a membrane stabilizing factor .
Ca++ conc. early opening of voltage
gated Na+ channels excitability