QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ortiz, C. Articles by Junge, D Search for Related Content PubMed Articles by Ortiz, C. Articles by Junge, D

Journal of Experimental Biology, Vol 75, Issue 1 171-187, Copyright © 1978 by Company of Biologists

JOURNAL ARTICLES

Depressant action of lithium at the crayfish neuromuscular junction: pre- and postsynaptic effects

CL Ortiz and D Junge

1. The effects of replacement of external sodium ions with lithium have been studied at the excitatory neuromuscular junction of the crayfish. 2. Intracellularly recorded excitatory junctional potentials fall 45% in amplitude in the first 10 min after lithium substitution, and fail irreversibly in 48--120 min. 3. The quantal content of extracellularly recorded excitatory junctional potentials declines 25--70% within the first 10 min of Li+ exposure. During the next 40--120 min the nerve terminal potentials and quantal release at individual synapses fail simultaneously and irreversibly. 4. The mean amplitude of the spontaneous miniature excitatory junctional potentials (m.e.j.p.s) is reduced 13% by Li+ substitution, but recovers upon restoration of sodium. The mean frequency of m.e.j.p.s rises steadily during Li+ exposure, and continues to increase after reintroduction of Na+. 5. The postsynaptic response to iontophoretically applied L-glutamate falls 35--40% in 10 min, but never falls below 45% of the control level. The effect on the glutamate response is completely reversible with sodium restoration. 6. The effective resistance of the postsynpatic cells is unaffected or only increased slightly by lithium substitution. 7. Thus, the primary mechanism of transmission block by lithium appears to be decreased transmitter release and inexcitability of presynaptic terminals, probably as a result of intracellular accumulation of lithium.

This article has been cited by other articles:

				A Pestronk and D. Drachman Lithium reduces the number of acetylcholine receptors in skeletal muscle Science, October 17, 1980; 210(4467): 342 - 343. [Abstract] [PDF]