Abstract

The physiological status of the neuromuscular junction of hibernating and nonhibernating 13-lined ground squirrels was studied to determine whether or not the metabolic changes during hibernation would alter the muscle's response to denervation. It was anticipated that the observations might clarify some aspects of the trophic interrelationship between nerve and muscle. The properties of innervated muscles were not significantly altered after the animals entered hibernation. The strength of contraction, speed of contraction, and resting membrane potential remained unchanged. In addition, extrajunctional sensitivity to acetylcholine did not develop. Because the muscles are inactive during hibernation, we conclude that muscle activity alone does not maintain the physiological properties of muscles. Denervation of muscles from nonhibernating animals resulted in loss of neuromuscular transmission, cessation of miniature end-plate potentials, partial muscle membrane depolarization, and appearance of extrajunctional sensitivity to acetylcholine. In contrast, muscles whose nerves were transected during the hibernating state showed unimpaired neuromuscular transmission and normal miniature end-plate potentials. However, the muscle became partially depolarized, indicating that the regulation of the resting membrane potential is under neurotrophic control and is not influenced solely by the release of acetylcholine (which had remained unchanged). The denervated muscles of hibernating animals did not develop extrajunctional sensitivity to acetylcholine; this probably reflects the low rate of protein turnover in tissues maintained at the low (7°C) body temperature of hibernating animals. Transection of the sciatic nerve of hibernating animals produced histologically demonstrable retrograde changes in the motor neurons of the lumbar spinal cord. It thus appears that hibernation does not adversely affect certain fundamental functions of the nervous system, such as transmission of nerve impulses, anterograde transmission of neurotrophic influences, and the retrograde transmission of signals which initiate the cell body's reaction to injury.

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