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Tutorial 2

Electrical changes
of Excitable
tissues
PREPERED BY :
r /Nahed El Sokkary
Dr /Siham Zakarya
Dr /Eman Helmy
Excitable tissues
• Excitable tissues respond to
different stimuli (electrical,
mechanical or chemical) when they
are excited.
• Example : Nerve fibers, muscle fibers.
Resting membrane potential
(RMP):
RMP in different excitable
tissues
• RMP in nerve fibers : –70 mv
• RMP in skeletal muscle: –90 mv
• RMP in cardiac muscle: –85 mv
• RMP in smooth muscle: –50 mv
Cause of RMP:

• RMP is caused by unequal distribution of


electrically charged ions on both sides of
the membrane with prevalence of
CATIONS ( Na+) at the outer surface, and
ANIONS at the inner surface (proteins).
Factors involved in production
of RMP
Selective permeability across
the cell membrane .
Sodium –Potassium Pump.
Na+ concentrated outside of cell
( (ECF
Sodium –potassium
pump:
Importance of Na+ -K+ pump:
• It maintains Na+ and K+ concentration
gradients across cell membrane.
• It establishes a negative electrical
potential inside cells
• Maintenance of the normal level of
intracellular K+ necessary for protein
metabolism.
• It keeps osmotic equilibrium to maintain
the cell volume.
Changes occurring in a
nerve activity
1. Electrical changes (Action Potential).
2. Excitability changes.
3. Metabolic changes.
4. Thermal changes (Heat production).
Electric
changes of the
nerve
Electrical changes
The electrical
changes
accompaning the
propagation of
excitation wave are
called the action
potential.
•Duration:2-4
msec
• velocity: 5
m/sec.
Phases of action potential
1. Latent period
• represents the time taken by the excitation wave
to travel from the site of stimulation to the
recording electrodes.
• No change in the membrane potential.
• Duration:1-3 msec
2. Spike potential
• Ascending limb : process of depolarization.
– Cause: Na+ influx
– Membrane depolarize -70→-55 mv (firing level)
• Rapid complete depolarization: -55 mv → zero
(isopotential).
• Reversal of polarity or overshoot: zero → +35 mv
• Descending limb : process of repolarization.
– Cause: K+ outflux
– The membrane potential falls rapidly towards
the resting level (repolarization).
After potentials
• Represent events that occur in the
nerve fiber after the passage of
excitation wave.
• Accompanied by changes in the
excitability of the nerve fiber.
• Excitability is increased during the
after depolarization and decreased
during the after hyperpolarization.
a(After depolarization:
• By after depolarization we mean
that the outer surface of the
membrane is more –ve than under
the resting condition ( lasts more
than 4msec( .
b( After hyperpolarization =
undershoot:
• After reaching the resting
level, the membrane becomes
slightly hyperpolarized i.e the
outerside of the membrane
becomes more positive than the the
innerside of the membrane
• Then, the membrane resumes its
resting potential gradually.
To summarize
3.Redistribution of ions inside and
outside
• Repolarization restores resting electrical
conditions of neuron, but does not restore
resting ionic conditions ( K+ is greater on
the outerside, Na+ is greater on the inner
side).
• Ionic redistribution is accomplished by
sodium-potassium pump following
repolarization.
Compound action potential:

• Stimulation of
mixed nerve trunk
causes a
compound action
potential, made up
of several waves
due to different
velocities of
conduction of
different fibers.
• The compound
action potential
has 3 main waves
A, B, and C.
Each wave belongs to a group
of fibers, group A conducts
faster followed by B, and lastly
C group.

The A group subdivided into


α , β , γ , and δ .
Faster fibers give spikes of
higher magnitude and shorter
duration according to the
Different types of nerve fibers.
Site Diameter Velocity of
conduction

Group A In somatic 3-20µ 15-120m/sec


myelinated
fibers

Group B Including small 1-3µ 5-13m/sec


myelinated,
Preganglionic
autonomic
fibers

Group C Including small 0. 3-1. 3µ 0. 5-3m/sec


non-
myelinated,
Somatic and
postganglionic
autonomic
fibers
Conduction of action potential
• Conduction of an action potential
excites adjacent portions of the
membrane.
• Types:
– Conduction in unmyelinated nerve
fibers
– Conduction in myelinated nerve
fibers (saltatory conduction):
Importance of saltatory
conduction:
• It increases velocity of conduction along
nerve fiber by the process of jumping. The
velocity of conduction is 3-120 m/sec.

• Depolarization is limited to the nodes of


Ranvier and so leakage of Na+ ions is
minimum to the inside of the fiber. This saves
the energy required by the sodium pump to
extrude sodium ions to the outside.
saltatory conduction

saltatory conduction
.
Result of action potential of the
nerve
• Depolarisation reaches
the nerve endings
• Ca+ ions enters the
nerve endings causing
the neurotransmitter
vesicles to fuse with
the membrane
• Release of
neurotransmitter in the
synaptic cleft
All or None Rule
• Stimulation of a single nerve fiber by a threshold
stimulus or over gives a maximal response and
no more.
• Subthreshold or subminimal stimulus gives no
response at all.
• The all or non rule can be applied also to the
single skeletal muscle fiber, cardiac muscle and
certain types of smooth muscles with gap
junctions. ( not whole skeletal muscle nor mixed
nerve trunk),
Local response or local
excitatory state:
• Subthreshold stimuli are not able to
produce an action potential, but they don’t
pass without any effect, they lead to:
1.Slight decrease in RMP (below firing level).
2.Slight increase in excitability (below level
which produces a response).
3.Application of multiple subthreshold
stimuli can be summated to give a
response ( when reaching to the firing
level), this is called temporal summation.
Three states of a neuron
Resting potential :
The state during which no nerve
impulse is being conducted although
the neuron is capable of doing so .
Action potential :
The state during which the neuron is
actively involved in conducting a
nerve impulse .
Recovery/Refractory potential :
The state during which the neuron is
unable to conduct a nerve impulse
since the neuron must “recover”
following the last nerve impulse .
Electric
changes of the
Skeletal muscle
Skeletal muscle
 voluntary

 Striated

Neurogenic

 Nerve-operated
Electrical changes in skeletal
muscle
Skeletal muscle Nerve

Resting membrane - 90 mv -70 mv


potential
Magnitude of action 130 millivolts (-90 to 105 mv ( -70 to +
potential +40 mv 35mv (
Duration of action 1- 5 msec 0. 5 - 1 msec
potential
Velocity of conduction 3-5 meters/second up to 120 meters/
sec

Duration of the after Longer Shorter


potentials
Generation of action potential in
Skeletal muscle
• Acetylcholine released from the nerve
ending diffuses into the synaptic cleft and
binds to the Ach receptors at the motor end
plate.
• Opening of ligand gated ion channels
• ( receptors of Ach)→influx of Na++ ions to
the interior of the muscle fiber→ generation
of AP at the fibers mid point→ AP travels in
both directions along sarcolemma.

• AP spreads to the depth of the
myofibrils via the T--tubular system
(extending from the sarcolemmal
membrane).
• Release of calcium ions from the lateral
sacs of the sarcoplasmic reticulum and
its diffusion to the thick and thin
filaments.
Relation of action
potential and Skeletal
muscle contraction
•The muscle spike
potential precedes
the muscle
contraction by
about 2 msec.

•It begins and


finishes before the
beginning of
muscle contraction
Motor Unit (All or non rule)
• Motor unit = Each anterior
horn cell together with its
axon and the number of
muscle fibers it supplies.
• When AHC is stimulated, all
its muscle fibers contract
• Each motor unit obeys the
all or non rule.
• The number of active motor
units increases, when the
intensity of stimulation of
the muscle increases
End plate potential
•Na + entry in muscle fiber ↓ membrane potential in
the local area of the end plate→ a local
unpropagated potential called the end plate potential
(EPP = partial depolarization of the membrane)
End plate potential (EPP)

• EPP is a local unpropagated potential


when it reaches a certain value called
threshold potential it fires the potential
on both sides of the motor end plate,
along the sarcolemmal membrane,
leading to muscular contraction.
Electric
changes of
the cardiac
muscle
Cardiac
Muscle
It is the most important muscle in
body.

 Involuntary

 Striated

 Myogenic

 Nerve-regulated
Cardiac Muscle

• Cardiac muscle fibers arranged in a


latticework, with gap junctions
between its fibers to conduct electric
activities at highest velocity.
• It is striated as skeletal muscle.
• The human heart beats about 100,000
times a day.

• Atrial and ventricular cells involved in this


contractile activity, referred to as
"working myocytes".

• These cells lack the ability to


spontaneously initiate their working cycle
and relay for their activation on external
trigger, the sinoatrial node.
• SAN myocytes set the rhythm and rate of
cardiac chamber contraction.

• “Pacemaker” cells generate repetitive action


potentials at a constantly controlled rate by
their inherited property of their membrane :
spontaneous Na+ leak generating the
prepotential or pace maker potential

• This prepotential propagates in the conducting


system of the heart causing the contractile
cardiac fibers to depolarise to generate the
action potential with plateau
Pathway of Electric activity
tribution of pacemaker activity in the heart tis
What gives pacemaker cells this ability?
• SAN myocytes
characterized as
having unstable
resting potential
which at the
termination of an
action potential ,the
membrane slowly
depolarizes until
threshold is reached
for a subsequent
action potential.
ace Maker Potential
• RMP in the pacemaker of the heart
is –60 mv.
• This is not enough negative voltage
to keep the sodium and calcium
channels totally closed.
• Therefore, the following sequence
occurs:
(1(Some sodium and calcium ions
flow inward “background current”.
(2(This increases the membrane
voltage to firing level of -45 mv .
Action potential with

plateau
The resting membrane
potential is about -85
millivolts, which rises in
depolarization up to +20
millivolts.

• Amplitude of action
potential : 105 millivolts.

• Membrane remains
depolarized for about 0.2
second, exhibiting a plateau
• Followed by abrupt
repolarization.
Phases of cardiac Action
potential
•initial rapid depolarization and the overshoot
(phase 0( are due to opening of voltage-gated Na+
channels leading to rapid Na+ influx

•The early rapid repolarization (phase 1( is due to


closure of Na+ channels and opening of K+ channel
producing transient outward K+ current.

• The plateau (phase 2( the flat portion of the


curve during which the membrane potential
remains near 0 mv is due to a slower but prolonged
opening of voltage-gated Ca2+ channels and
delayed opening of K+ channels.
•Final repolarization (phase 3( is
due to closure of the Ca2+
channels and a slow, delayed
increase of K+ efflux through
various types of K+ channels.

• The resting membrane


potential (phase 4(
To summarise
Pace-maker AP Cardiac fibre AP
Response Slow response AP Rapid response AP

RMP - 60 mv - 85 mv

Firing level - 45 mv - 70 mv

Max dep + 10 mv +30 mv

Magnitude of AP 70 mv 120 mv

Depolarisation Begins by Na+ influx Na+ influx


& continues by Ca+2
influx

Plateau No Plateau dt slow


Ca+2 channel
activation
Electric
changes of
the Smooth
muscle
Smooth muscle
 Involuntary

 Not Striated (plain)

Myogenic

 Regulated
Visceral smooth muscle ( unitary )
• Found in walls of digestive tract, urinary tract ,
genital tract and many blood vessels.
• Visceral smooth muscles are characterized by
presence of gap junctions between the various
cells or fibers.
• So once an action potential is generated in one
muscle fiber, it spread to all the adjacent
fibers, leading to spontaneous contraction
(act in a syncytial fashion)
• It is mainly controlled by non-nervous
stimuli.
Multi-units smooth muscle
• Present in the muscle lining the blood
vessels, ciliary muscle , iris of the eye,
and the piloerector muscle
• They are made of separate muscle fibers,
each fiber responds independent from the
other (Non syncytial).
• This type of muscle is controlled by nerve
signals from the autonomic nervous
system.
Electric changes in Visceral smooth
muscles
• RMP of smooth muscle cells is -50 mV.
• In contrast to nerves and skeletal muscle
cells, the membrane potential of certain
smooth muscle cells fluctuates
spontaneously between 5 to 15 mV those
are called pace-makers due to spontaneous
Na+ leak through their membranes .
• Because the cells are electrically
coupled (by gap junctions in unitary
cells), these fluctuations in membrane
potential spread to adjacent muscle
cells, resulting in what are called "slow
waves" = waves of partial
depolarization in smooth muscle.
Electric changes in smooth muscles
slow waves can not elicit contractions (<35
mv) but they coordinate muscle
contractions by controlling the appearance
of a second type of depolarization event -
"spike
potentials”.
Electric changes in smooth muscles
• Spike potentials are true action potentials
with 10-50 msec duration that elicit muscle
contraction.
• They result when a slow wave passes over
an area of smooth muscle primed by
exposure to neurotransmitters released in
response to local stimuli, including
distension of the wall of
the digestive tube
Example: what happens when a large bolus
of ingested food enters the small intestine

• The bolus distends the gut, stretching its


walls.
• Stretching stimulates nerves in the wall of
the gut to release neurotransmitters into
smooth muscle at the site of distension - the
membrane potential of that section of
muscle becomes "more depolarized."
• When a slow wave passes
over this area of sensitized
smooth muscle, spike
potentials form and
contraction results.
• The contraction moves
around and along the gut in
the coordinated manner
because the muscle cells are
Summary: electric changes in
smooth muscles
• Basic patterns of electrical activity across
the membranes of smooth muscle cells
– Slow waves
– Spike potentials.
– AP with plateau in the vascular smooth
muscles, ureter, and uterus.

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