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Excitability changes in crayfish motor neurone terminals
Author(s) -
Zucker Robert S.
Publication year - 1974
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1974.sp010643
Subject(s) - chemistry , depolarization , hyperpolarization (physics) , biophysics , motor nerve , axon , excitatory postsynaptic potential , calcium , neuroscience , biology , biochemistry , receptor , organic chemistry , nuclear magnetic resonance spectroscopy
1. Changes in the post‐activation excitability of crayfish motor nerve terminals were used to measure afterpotentials that might be related to facilitation of transmitter release. 2. The refractory period is followed by a period of supernormal excitability in which the threshold of nerve terminals drops to about 70% of its pre‐activation level at about 15 msec following an impulse. The threshold returns exponentially to its pre‐activation level with a time constant of about 25 msec at 13° C. Such a supernormal excitability is rarely seen in pre‐terminal nerve branches or in the main axon. 3. Following a brief high‐frequency tetanus the peak of the supernormal excitability is greater than that following a single impulse. At low temperature this peak is reduced and delayed, and the decay rate of the supernormal excitability is prolonged with a Q 10 of about 2·5. 4. Depolarization of nerve terminals decreases, and hyperpolarization increases, the magnitude of the post‐activation supernormal excitability. 5. The magnitude of the supernormal excitability depends on the external potassium concentration, but not on sodium. In low calcium the peak supernormal excitability is often reduced. High calcium concentration and manganese ions have no effect, but cobalt abolishes the supernormal excitability, and its effects are only slightly reversible. Both cobalt and manganese reversibly block neuromuscular transmission. 6. Strophanthidin has no effect on the post‐activation supernormal excitability, but proteolytic enzymes reduce or abolish it, and hyperosmotic solutions also affect it. 7. It is suggested that the action potential is followed by a depolarizing afterpotential in nerve terminals which is caused by a transient increase in the potassium concentration around the terminals. There is no evidence that afterpotentials in nerve terminals are related to facilitation in any way.