Neuromuscular junction, a. Diagram of a neuromuscular junction. An axon is shown making contact with a muscle cell. Note how the junctional folds of the muscle cell augment the surface area within the synaptic cleft. The external lamina extends throughout the cleft area. The cytoplasm of the Schwann cell is shown covering the axon terminal. (Modified from Kelly DE, Wood RL, Enders AC, eds. Bailey's Textbook of Microscopic Anatomy. Baltimore: Williams & Wilkins, 1984.) b. Electron micrograph of a neuromuscular junction shows the axon ending within the synaptic cleft of a skeletal muscle fiber. An aggregation of mitochondria (M) and numerous synaptic vesicles (SV) is visible. The portion of the motor axon ending that is not in apposition to the muscle fiber is covered by Schwann cell cytoplasm (5), but no myelin is present. The muscle fiber shows the junctional folds (JF) and the subneural clefts (SnC) between them. The external lamina of the muscle fiber is barely evident within the subneural clefts. Other structures present are the aggregated mitochondria of the muscle fiber (M) in the region of the neuromuscular junction, the nucleus (N) of the muscle fiber, and some myofibrils (MF). x32,000. (Courtesy of Dr. George D. Pappas.)
then binds to acetylcholine receptors on the sarcolemma. This binding opens cation channels associated with the acetylcholine receptors, causing an influx of Na+. The influx of Na+ results in a localized membrane depolarization, which in turn leads to the events described above. An enzyme called acetylcholinesterase quickly breaks down the acetylcholine to prevent continued stimulation.
The muscle fiber cytoplasm that underlies the junctional folds contains nuclei, many mitochondria, rough endoplasmic reticulum (rER), free ribosomes, and glycogen. These cytoplasmic organelles are believed to be involved in the synthesis of specific acetylcholine receptors in the membrane of the cleft, as well as acetylcholinesterase.
A neuron along with the specific muscle fibers that it innervates is called a motor unit
A single neuron may innervate several to a hundred or more muscle fibers. Muscles capable of the most delicate movements have the fewest muscle fibers per motor neuron in their motor units. For example, in eye muscles, the innervation ratio is about one neuron to three muscle
fibers; in the postural muscles of the back, a single neuron may innervate hundreds of muscle fibers.
The nature of muscle contraction is determined by the number of motor neuron endings as well as by the number of specific type of muscle fibers that are depolarized. Although depolarization of a muscle fiber at a single neuromuscular junction is characterized as an "all-or-none" phenomenon, not all nerve terminals discharge at once, which allows a graded response to the contractile stimulus. Loss of innervation produces muscle fiber (and muscle) atrophy as well as total loss of function in the dener-vated muscle.
Innervation is necessary for muscle cells to maintain their structural integrity
The motor nerve cell not only instructs the muscle cells to contract but also exerts a trophic influence on the muscle cells. If the nerve supply to a muscle is disrupted, the muscle cell undergoes regressive changes known as tissue atrophy. The most conspicuous indication of this atrophy is thinning of the muscle and its cells. If innervation is reestablished surgically or by the slower process of natural regeneration of the nerve, the muscle can regain normal shape and strength.
The events leading to contraction of skeletal muscle can be summarized as a series of steps
The events involved in contraction can be summarized as follows (the numbers refer to the numbers in Fig. 10.10):
1. The contraction of a skeletal muscle fiber is initiated when a nerve impulse traveling along the axon of a motor neuron arrives at the neuromuscular junction.
2. The nerve impulse prompts the release of acetylcholine into the synaptic cleft, which causes local depolarization of sarcolemma.
Myasthenia gravis is an autoimmune disease characterized by extreme muscle weakness. In this disease, the acetylcholine receptors on the sarcolemma are blocked by antibodies to the receptor protein. Thus, the number of functional receptor sites is reduced, weakening the muscle fiber response to the nerve stimulus. As the disease progresses, the number of neuromuscular junctions is reduced. Abnormalities within the synaptic cleft (e.g., widening of the synaptic cleft, disappearance of junctional folds) also occur, further reducing the effectiveness of the muscle fibers.
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