Flashcards in Chapter 7 - Guyton Deck (19):
Muscle fibers are innervated by nerve fibers that originate in the ______ horns of the spinal cord.
Smaller folds at the muscle membrane which greatly increase the surface area at which the synaptic transmitter can act.
These insulate the motor end plate from the outside environment.
What is the reason for increased mitochondria at the axon terminal?
will supply ATP for synthesis of the excitatory neurotransmitter acetylcholine
the synaptic space contains this enzyme which will destroy acetylcholine very soon after is has been released from the synaptic vesicles in order to stop transmission
What is the stimulus for the release of Ach from the vesicles?
located next to the dense bars are voltage gated Ca channels, when an AP occurs, these open and Ca will then diffuse into the synaptic cleft
General characteristics of Ach receptors on muscle fiber membrane.
protein complex made of 5 subunit proteins (2 alpha , 1 beta, 1 delta and 1 gamma), main effect of the opening of Ach channels is the influx of sodium, allowing a local positive potential change called the end plate potential - this will initiate an action potential spreading through the muscle fiber and causing a muscle contraction
How long is Ach in the synaptic cleft?
Ach only stays in the synaptic cleft for a few milliseconds which is enough to excite the muscle fiber, the rapid removal prevents continued muscle re-excitation after the muscle fiber has recovered from its initial AP
End Plate Potential
sudden influx of Na through the Ach channels causes the electrical potential inside the fiber at the local area of the end plate to increase in the positive direction about 50 to 75 millivolts, creating the end plate potential - this is enough to initiate an AP
Two examples of weak end plate potentials.
can be caused by the drug curare - a drug that blocks the gating action of Ach on their channels by competing for the receptor sites; it can also be caused by botulinum toxin - a poison that decreases the Ach release by the nerve terminals
What is meant by the "high safety factor" of the NMJ?
each impulse that comes to the neuromuscular junction causes about three times as much end plate potential as is really needed to stimulate the muscle fiber
What occurs during neuromuscular fatigue?
stimulation of the nerve fiber at rates higher than 100 times per second for several minutes will diminish the number of Ach vesicles to where the impulses will fail to pass through the fiber; same thing that happens in the CNS when synapses are overexcited (this is very rare and only happens at exhausting levels of activity)
Stages of the formation and release of Ach at the neuromuscular junction:
1) vesicles are formed by the golgi apparatus in the motor neuron in the spinal cord, they are transported by axoplasm to the NMJ, they collect in the nerve terminals of a single skeletal muscle end plate 2) Ach is synthesized in the cytosol of the nerve fiber terminal and then transported into the vesicles 3) AP arrives at the nerve terminal, Ca channels open, increasing the amount of Ca inside which causes a higher rate of fusion of Ach vesicles with the terminal membrane, the vesicles rupture, causing exocytosis of Ach into the synaptic space, Ach is split by acetylcholinesterase, with part of it (choline) returning to the nerve terminal to be reused to make more Ach 4) a few seconds after each action potential, “coated pits” appear in the nerve terminal caused by contractile proteins like clathrin, which is attached to the areas where the original vesicles were, the proteins will contract and cause the pits to break away to the interior of the membrane, forming new vesicles, then a few seconds later Ach is transported to these vesicles and the cycle restarts
Drugs that Stimulate the Muscle Fiber by Ach-Like Action
metacholine, carbachol, nicotine have the same effect on the muscle fiber that Ach does but are not destroyed by acetylcholinesterase
Drugs that Stimulate the Neuromuscular Junction by Inactivating Acetylcholinesterase
neostigmine, physostigmine and diisopropyl fluorophosphate (all are lethal)
Drugs that Block Transmission at the Neuromuscular Junction
curariform drugs can prevent passage of impulses from the nerve ending into the muscle, D-tubocurarine blocks the action of Ach binding to its receptor, preventing the channels from initiating an AP
causes muscle paralysis because of the inability of the NMJs to transmit enough signals from the nerve fibers to the muscle fibers, believed that myasthenia gravis is an autoimmune disease in which the patient have developed immunity against their own Ach activated ion channels - their antibodies attack the ach gated sodium ion channels, end plate potentials are too weak to stimulate muscle fibers, can cause paralysis of the respiratory muscles causing death, patients take neostigmine or another anticholinesterase drugs which will allow a large amount of Ach to accumulate in the synaptic space
What is the difference between a muscle fiber action potential and a nerve fiber action potential?
resting membrane potential is about -80 to -90 mV, duration of the AP is 1 to 5 milliseconds; 5 times longer than nerves, velocity of conduction is 3 to 5 m/sec; 1/13 of the velocity of conduction in large myelinated nerve fibers that excite skeletal muscle (duration is long but velocity is slower)