Development of the Neuromuscular Junction

Abstract

To determine the effects of nerve explants on the integrity of motor end plates in vitro, cholinesterase activity and structure of end plates were compared in newt muscle denervated in vivo, cultured in the absence of nerve explants, and cultured in the presence of sensory ganglia . In neuromuscular junctions denervated in vivo or in vitro, the synaptic vesicles become clumped and fragmented . A few intact vesicles escape into the synaptic cleft . Axon terminals degenerate until they are left as residual bodies within the Schwann cell cytoplasm . functional folds on the muscle surface are reduced in height and are no longer evident once traces of axoplasm within the Schwann cell disappear. End plate cholinesterase activity is reduced as junctional folds are lost . When muscle is cultured in the presence of a sensory ganglion, the terminal axoplasm degenerates in the same manner but junctional folds persist on the muscle surface. Moderately intense cholinesterase activity remains in association with the junctional folds, so that normal motor end plates are maintained in the absence of innervation . These results show that degenerative changes in the structure of the motor end plate and loss of cholinesterase activity occurring in organ culture as a result of denervation can be retarded by nerve explants that do not directly innervate the muscle .

Concentration of Caveolin-3 at the Neuromuscular Junction in Young and Old Rat Skeletal Muscle Fibers

“…Similarly, after denervation the axon terminals degenerate within a day or two, and by 3 days the postsynaptic apparatus already shows significant degenerative changes, in particular a reduction in the height and complexity of the postsynaptic folds (Brown et al 1982;Lentz 1972;Pulliam and April 1979). In these earlier studies, no comment was made on the effect of denervation on the caveolar content of the postsynaptic membrane.…”

Histochemical and electron microscopic observations on the myoneural junctions of rats with carbon disulfide induced polyneuropathy.

“…Weakening of the enzyme activity was seen only occasionally in some myoneural junctions, a finding consistent with denervation (7) as evidenced by ultrastructural observation of myoneural junctions with advanced degeneration or total destruction of the terminal axons. In these myoneural junctions alterations in the postsynaptic membrane also occurred which may be attributed to denervation-like changes (18).…”

Neural control of skeletal muscle cholinesterase: a study using organ‐cultured rat muscle.

“…Selective interruption of axonal transport by subepineural application of colchicine to cat hypoglossal nerve has been shown to cause a large decrease in end-plate ChE in the geniohyoid muscle, and this result has been interpreted to mean that there are trophic substances) moved by axonal transport which normally maintain endplate ChE (Fernandez & Inestrosa, 1976). Several studies have shown that the ChE 502 NEURAL CONTROL OF CHOLINESTERASE of cultured muscle can be influenced by a variety of neural explants and extracts (Lentz, 1971(Lentz, , 1972(Lentz, , 1974aOh, Johnson & Kim, 1972;Oh, 1975Oh, , 1976. These studies are of considerable interest because they raise the possibility that cultured muscle may be used to assay trophic substances) normally delivered by nerve to maintain muscle ChE, but they are difficult to interpret because little evidence has been obtained to establish that the changes induced in muscle ChE in culture are due to physiologically relevant trophic substances) and not to non-specific factors.…”