Electrical changes of Excitable tissues

Tutorial 2

Dr /Nahed El Sokkary

Dr /Siham ZakaryaDr /Eman Helmy

PREPERED BY :

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.

NaNa++ concentrated outside of cell (ECF) concentrated outside of cell (ECF) KK++ concentrated inside cell (ICF) concentrated inside cell (ICF)

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 potential1. 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.

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 , , , and .Faster fibers give spikes of higher magnitude and shorter duration according to the diameter of the fibers.↑ diameter→ ↑ velocity of conduction

Site Diameter Velocity of conduction

Group A In somatic myelinated fibers

3-20

15-120m/sec

Group B Including small myelinated, Preganglionic autonomic fibers

1-3 5-13m/sec

Group C Including small non-myelinated, Somatic and postganglionic autonomic fibers

0. 3-1. 3

0. 5-3m/sec

Different types of nerve 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.

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 .

Three states of a neuron

Electric changes of the Skeletal muscle

Skeletal muscle

voluntary• Striated

Neurogenic

Nerve-operated

Electrical changes in skeletal muscle

Skeletal muscle Nerve

Resting membrane potential - 90 mv -70 mv

Magnitude of action potential 130 millivolts (-90 to +40 mv 105 mv ( -70 to + 35mv )

Duration of action potential 1- 5 msec 0. 5 - 1 msec

Velocity of conduction 3-5 meters/second up to 120 meters/ sec

Duration of the after potentials

Longer Shorter

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 MuscleIt 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

Distribution of pacemaker activity in the heart tissue

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.

• 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 .(3) At this level an action potential is generated and

the cycle is repeated.

Pace Maker Potential

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.

• 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.

Phases of cardiac Action potential

•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)

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 & continues by Ca+2 influx Na+ influx

Plateau No Plateau dt slow Ca+2 channel activation

To summarise

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 electrically coupled through gap junctions.

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.