3rd lecture on nerve physiology by Dr. Roomi.pptx
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Transcript of 3rd lecture on nerve physiology by Dr. Roomi.pptx
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7/29/2019 3rd lecture on nerve physiology by Dr. Roomi.pptx
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Nerve physiology3rd lecture
By
Dr. Mudassar Ali Roomi (MBBS, M. Phil)
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Inhibition of Excitability-
Stabilizers and Local Anesthetics
the factors that decreasenerve excitability arecalled as membrane-stabilizing factors.
Calcium
local anesthetics: Examples: procaine and
tetracaine.
Mechanism of action of localanesthetics: acts directly onthe activation gates of thesodium channels, making itmuch more difficult for thesegates to open.
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Role of calcium in membrane excitability
Hypercalcemia decreasemembrane excitability.***
In hypercalcemia decreasedexcitability of membrane (alsosevere constipation).**
Hypocalcemia increasedexcitability of nervous tissue.**
Inner side of sodium channels ishighly negatively charged.
Calcium ions bind with negativeinner surface of sodium
channels complete closure ofactivation gates of thesechannels at rest.
So, Calcium (normal levels)st
abilizes the membrane anddecreases its exciability.
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Why tetany occurs in hypocalcemia??
Decreased calcium in ECFno complete closure ofactivation gates ofsodium channels at rest
sodium ions leak intomembrane from ECFhypo-polarization(membrane potential
becomes less negative &near to threshold) & onslight stimulationaction potential (tetany).
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Why tetany is aggravated in alkalosis?
Protein molecules behaveas acid (proton donorsbecome anions) inalkaline pH.
At 7.4 (alkaline body pH),protein anions bindpositive ions (sodium,potassium, calcium).
Protein bound form of
calcium increases & ionicform thus decreasestetany.
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NERVE FIBER /SKELETAL MUSCLE
CARDIAC
MUSCLE
SMOOTH
MUSCLE
Multiple peripheral
nuclei.
Single central
nucleus.
Single central
nucleus.
Triad is at the
junction of A & Ibands.
Intercalated discs /
gap junctions are atthe level of Zmembranes. (Diad)
In some places
(intestine), randomlydistributed thick &thin filamentsinterdigitate.
Few mitochondria.Major source of energyis CHO.
Glycolysis Citric acid
cycle.
More mitochondria
(25% mass). Majorsource of energy isfat (60%) at rest.
Fewer mitochondria.Mostly glycolyticmetabolism.
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Propagation of action potential
Propagation of actionpotential is an exampleof positive feedbackmechanism.
velocity (m/sec) ofmyelinated fiber =diameter (in mm) x 4.5
velocity of (m/sec)unmyelinated fiber =Square root of diameter
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Propagation of action potential in
un-myelinated nerve fibers
Point to point conduction. Local circuit of current is formed
between depolarized point &adjacent polarized point.
Current flowing out throughdepolarized point, activates Na+
channels at polarized pointdepolarization action potential.
Then a new circuit of current isformed between this depolarizedpoint & adjacent polarized point.
In case of unmyelinated nervefiber, velocity of conduction isslow, because it is point to point.
Synapses only allow propagationbetween pre synaptic to postsynaptic neuron inside the body(law of forward conduction). butin vitro it is in both directions.
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Myelination
Schwann cells surround the nerve
axon forming a myelin sheath
Sphingomyelin decreases
membrane capacitance and ion flow5,000-fold
Sheath is interrupted every 1-3 mm
: node of Ranvier
Figure 5-16; Guyton & Hall
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Propagation of action potential
along a myelinated nerve fiber
SALTATORY CONDUCTION
Saltare: to jump
Node to nodeconduction.
Internodes aremyelinated and act asinsulators.
Myelin sheath is absent
at the nodes of Ranvier& neurilemma at thenodes has got ionchannels.
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Local circuit of saltatory conduction
depolarized node
adjacent polarized node
conduction of
current throughaxoplasm and ECF
next node is also
depolarized
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Benefits of saltatory conduction
1. Faster velocity ofconduction in largemyelinated nerve fiberse.g A-alpha fibers (120m/sec ). It is very slow(0.5-2 m/sec) in smallunmyelinated nervefibers e.g. type C fibers.
2. Less energy expenditure
due to less ionic change3. Insulation of nerve fibersprevents the shortcircuiting.