Transcript Document

Seventh lecture
Changes occurring in the nerve as a result of conduction of a
nerve impulse:
I- Electrical changes
II- Excitability changes
It passes in the following phases:
a- Temporal rise of excitability is associated with the local
b- Absolute refractory period (ARP)
c- Relative refractory period (RRP)
During this period the excitability of the nerve is partially recovered.
Stronger stimuli are needed to excite the nerve.
During this period, the gates of K+ channels are opened and the
membrane is in the process of depolarization. The magnitude of the
second action potential is less than normal.
d- Supernormal phase of excitability
The excitability is above normal i.e. weaker stimuli can excite the
nerve fibers.
e- Subnormal phase of excitability:
The excitability is below normal i.e. stronger stimuli are needed to excite
the nerve fibers.
III- Metabolic changes
The nerve contains the enzymes responsible for
glycolysis, citric acid (Kreb’s) cycle and electron
transport (cytochrome oxidase). Thus the nerve can
generate and store energy in the form of ATP.
IV- Thermal changes
1- Initial heat.
2- Delayed heat.
Factors affecting the excitability and
conductivity of the nerve fibers
1- Physical factors
Thermal:
Warming increases while cooling decreases the
excitability by decreasing the metabolic reac tions
need for the Na – K pump. Inhibition of Na-K pump
leads to accumulation of the Na+ ions inside the
nerve fibers which decreases the membrane potential
and lastly leads to loss of the resting membrane
potential i.e. loss of excitability and conductivity.
Mechanical:
Deep pressure on the nerve fibers decreases
the excitability and conductivity of these fibers.
2- Chemical factors
Local anaesthetic drug as cocaine, novocaine & xylocaine
decrease the membrane permeability to Na+ ions (by
blocking the Na+ channels). Thus, depolarization is
inhibited and consequently the nerve impulse fail to be
generated and conducted.
Ions
Ca++ ions:
1-Increased Ca++ ions decreases excitability of the nerve fibers by
decreasing the
membrane permeability to Na+ ions and increasing the threshold of
stimulation.
2-Decreased Ca++ ions increases excitability by increasing Na+
permeability and
decreasing the threshold of stimulation.
Na+ ions:
1-Increased Na+ ions increases excitability by facilitating the
process of
depolarization.
2-Decreased Na+ ions decreases excitability by delaying the
process of
depolarization.
K+ ions:
-Increased K+ ions in the extracellular fluid increases excitability becusae K+
ions diffuse inside the nerve fiber producing depolarization (like Na+ ions).
-Decreased K+ ions in the extracellular fluid decreases excitability because K+
ions diffuse from inside to outside the nerve fibers producing
hyperpolarization.
O2 lack and CO2 excess decreases excitability.
H+ ion concentration: Alkalinity increases, while acidity decreases excitability.
3- Electrical factors
In electrotonus electrotonic potential, the anelectrotonus
decreases while the catelectrotonous increases the
excitability.
Nerve block
It means failure of conduction of nerve impulses from one place to another. It
also means failure of excitability of the nerve fibers i.e. there is no generation or
propagation of nerve impulses. Nerve block can be produced by:
1- Physical causes:
a-Thermal: Sever cooling.
b-Mechanical: Deep pressure.
c-Injury or crushing of the nerve fibers.
2- Chemical causes (membrane stabilizers):
a-Local anaesthetic drugs.
b-Increased Ca++ ions.
c-Decreased Na+ ions.
d-Decreased K+ ions.
3- Electrical causes:
Strong anelectrotonus.
Neuro-musclular junction
Since the number of fibers in the muscle greatly exceeds, the number
of fibers in the motor nerve .
Each nerve fiber branches many times and stimulates a variable
number of muscle fibers.
A single motor neuron innervates many muscle fibers.
A motor neuron, plus the muscle fibers supplied by a motor unit which
perform fine and delicate movements, a few muscle fibers are supplied
by one motor neuron
While in muscles used for rapid coarse movements, many
muscle fibers are supplied by a single neuron.
The nerve ending makes a junction called the
neuromuscular junction.
Physiological anatomy of the neuromuscular junction
Near the surface of the muscle, the motor nerve
fiber loses its myelin sheath and divides into many
branches, each branch forms a junction with a single
muscle fiber. The terminal part of the axon lies in a shallow
groove on the surface of the muscle fiber. The axon
terminal contains small vesicles that carry acetylcholine
which is the chemical transmitter at the neuromuscular
junctions.
The presynaptic terminals contain
a large number of mitochondria.
The terminal part of the axon is separated from the muscle plasma membrane
by a space known as the synaptic cleft.
The post-synaptic membrane is the plasma membrane of the muscle fiber.
It is called the motor end plate. The surface area of this membrane is greatly
increased by the presence of numerous folds of the membrane called the
junctional folds. The post-synaptic membrane contain the receptors for the
chemical transmitter acetylcholine (cholinergic receptors). These receptors are
complex protein molecules that have a double functions. Each receptor has:
(1)binding site for acehylcholine
(2) an ion channel.
The membrane of the motor end plate contains also an enzyme called
cholinestrase. This enzyme is essential for breaking down the
acetylcholine to an inactive form once it has done its action.
Mechanism of neuro-muscular transmission
When nerve impulse in a motor neuron reaches the axon terminal, it
opens the voltage sensitive Ca++ channels, and thus allowing the Ca++ ions to
diffuse into the axon terminal. The increase in the intracellular Ca++ ion causes
the synaptic vesicles that contain acetylcholine to move towards the membrane,
fuse with it, and lastly to rupture and release its content into the synaptic cleft.
Acetylcholine diffuses across the cleft to the postsynaptic membrane, where it
combines with the specific binding sites on the receptor. When the binding
occurs, the membrane channels becomes permeable to both Na+ and K+ ions
at the same time. Because of the differences in electrochemical gradients
across the membrane, more Na+ move in, than K+ moves out, producing a
local depolarization of motor end plate known as the motor end plate potential.
The end plate potential causes small local currents which
depolarize the adjacent muscle plasma membrane to the
threshold level for generation of an action potential.
This action potential propagates on both sides of the motor
end plate to the whole length of the muscle fiber leading to
its contraction.
After passage of the action potential, the muscle
membrane repolarizes and returns to its resting
potential.