Physio Ch 07 Flashcards
formed by the nerve fiber through invagination into the surface of the muscle fiber present in plasma membrane
branching nerve terminals
innervated by large, myelinated nerve fibers that originate from large motoneurons in the anterior horns of the spinal cord
skeletal muscle fibers
schwann cells insulate this structure from surrounding fluids
motor end plate
invaginated membrane between an axon terminal and muscle fiber membrane
synaptic gutter or synaptic trough
space between the axon terminal and muscle fiber membrane
synaptic space or synaptic cleft
folds at the bottom of synaptic gutter greatly increasing the surface area at which the synaptic transmitter can act
subneural clefts
where does acetylcholine get synthesized
cytoplasm of the axon terminal
destroys acetylcholine a few milliseconds after it has been released from the synaptic vesicles
acetylcholinesterase
neural membrane empty their acetylcholine into the synaptic space by the process of
exocytosis
located almost entirely near the mouths of the subneural clefts lying immediately below the dense bar areas
acetylcholine-gated ion channels
these positive ions flow through acetylcholine gated channels more than any other ions
sodium ions
Why do sodium ions flow through acetylcholine-gated channel more than potassium and calcium?
- There are only two positive ions in large
concentration: sodium ions in the extracellular fluid and potassium ions in the intracellular fluid. - The negative potential on the inside of the muscle membrane, −80 to −90 millivolts, pulls the positively charged sodium ions to the inside of the fiber, while simultaneously preventing efflux of the positively charged potassium ions
when they attempt to pass outward
this initiates an action potential that spreads along the muscle membrane and causes muscle contraction
end plate potential
Mechanisms of destruction of released acetylcholine (2)
(1) Most of the acetylcholine is destroyed by the enzyme acetylcholinesterase,
(2) A small amount of acetylcholine diffuses out of the synaptic space and is then no longer available to act on the muscle fiber membrane
a drug that blocks the gating action of acetylcholine on the acetylcholine channels by competing for the acetylcholine receptor sites
curare
bacterial poison that decreases the quantity of acetylcholine release by the nerve terminals
botulinum toxin
stimulation of the nerve fiber at rates greater than 100 times per second for several minutes often diminishes the number of acetylcholine vesicles so much that impulses fail to pass into the muscle
fatigue
enumerate these drugs having the same effect on the muscle fiber as does acetylcholine
methacholine, carbachol, and nicotine
enumerate the drugs which inactivate the acetylcholinesterase in the synapses so that it no longer hydrolyzes acetylcholine
neostigmine, physostigmine, and diisopropyl fluorophosphate
powerful “nerve” gas poison and inactivates acetylcholinesterase for weeks
diisopropyl fluorophosphate
combine with acetylcholinesterase to inactivate the acetylcholinesterase for up to several hours
Neostigmine and physostigmine
prevent passage of impulses from the nerve ending into the muscle
curariform drugs
a drug that blocks the action of
acetylcholine on the muscle fiber acetylcholine receptors
D-tubocurarine
causes muscle paralysis because of inability of the neuromuscular junctions to transmit enough signals from the nerve fibers to the muscle fibers
myasthenia gravis
an autoimmune disease in which the patients have developed antibodies that block or destroy their own acetylcholine receptors
Myasthenia gravis
nerve ending of skeletal muscle fibers make a junction with muscle fiber near its midpoint
neuromuscular junction
When a nerve impulse reaches the neuromuscular junction, how many vesicles of acetylcholine are released
from the terminals into the synaptic space
125 vesicles
located near mouths of the subneural clefts lying immediately below the dense bar areas
acetylcholine-gated ion channels
protein complex composed of two alpha proteins and one each of beta, delta, and gamma proteins
acetylcholine receptors
do not pass through acetylcholine gated channel due to strong negative charges in the mouth of channel
chloride ions
Ach is rapidly removed by 2 mechanisms
(1) Most of the acetylcholine is destroyed by the enzyme acetylcholinesterase
(2) A small amount of acetylcholine diffuses out of the synaptic space
an increase by millivolt of nerve membrane that is sufficient to initiate more and more sodium channel to open, causing action potential
20 to 30 millivolts
increase to about 50-70 millivolts at the local area of the end plate results to
local potential or end plate potential
diminishes number of Ach vesicle resulting impulse to fail to pass into the muscle fiber
stimulation of the nerve fiber at rates greater than 100 times per second for several minutes
Acetylcholine is synthesized in
cytosol of nerve fiber terminal
formed by the Golgi apparatus in the cell body of the motoneuron in the spinal cord
small vesicles
occurs in about 1 in every 20,000 characterized by inability of the neuromuscular junctions to transmit enough signals from the nerve fibers to the muscle fibers
myasthenia gravis
Resting membrane potential in skeletal fibers
-80 to -90 millivolts
Duration of action potential of skeletal muscles
1 to 5 milliseconds
velocity of conduction in skeletal muscle
3 to 5 m/sec
current penetrate deeply into muscle fiber through this structure, which also transmits the action potential
transverse tubules
small and run transverse to the myofibrils
T tubules
branch among themselves and form entire planes interlacing among all the separate myofibrils
T tubules
communicate with the ECF surrounding the muscle fiber and contain extracellular fluid in their lumen
T tubules
internal extension of the cell membrane
T tubules
Sarcoplasmic reticulum is composed of?
(1) large chambers called terminal cisternae that abut the T tubules
(2) long longitudinal tubules that surround all surfaces of the actual contracting myofibrils
One of the special features of the sarcoplasmic reticulum
excess of calcium ion in high concentrations
As action potential reaches the T tubule, the voltage change is sensed by
dihydropyridine receptors
dihydropyridine receptors are linked to?
calcium release channels or ryanodine receptor channels
Activation of dihydropyridine receptors triggers the opening of
calcium release channels in the cisternae
a protein present inside the reticulum that can bind up to 40 times of more calcium
calsequestrin
total duration of this calcium “pulse” in the usual skeletal muscle fiber lasts about
1/20 of a second
