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The Effects of Electroshock Convulsions on Calcium Transport within Synaptic Terminals
Author(s) -
DelgadoEscueta A. V.,
Victor S.,
Davidson D.
Publication year - 1980
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1980.tb09953.x
Subject(s) - convulsion , calcium , sodium , chemistry , medicine , in vivo , efflux , endocrinology , synaptosome , anesthesia , epilepsy , biology , biochemistry , neuroscience , microbiology and biotechnology , organic chemistry
Calcium transport was assessed within synaptic terminals isolated from cerebral cortices of rats which experienced one maximal electroshock (ES) convulsion daily. No significant change in calcium content [(Ca 1 )] of synaptosomes was present after 2 consecutive days of maximal convulsions. After 4 and 6 days of maximal seizures, (Ca 1 ) rose 20% and 37%, respectively. 15 Ca 2+ influx within synaptosomes in vitro increased after 6 days of ES convulsions (1.94 ± 0.4 μmol/g protein/min in ES convulsions versus 1.54 ± .03 μmol/g protein/min in controls). The higher rate of 45 Ca 2+ influx in convulsed animals was accounted for by elevated internal sodium [(Na 1 )] values. Maximal 45 Ca 2+ efflux decreased after ES convulsions (0.48 μmol/g protei/min in ES convulsions versus 0.8 μmol/g protei/min in controls). The slower rate of 45 Ca 2+ efflux after convulsions was also accounted for by elevated (Na 1 ). Our results suggest that (Ca 1 ) increased within synapses after in vivo ES convulsions secondary to a primary ionic event, namely, elevated (Na 1 ).