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Chronic diazepam treatment in rats causes long‐lasting changes in central [ 3 H]‐5‐hydroxytryptamine and [ 14 C]‐γ‐aminobutyric acid release
Author(s) -
Hitchcott P.K.,
File Sandra E.,
Ekwuru M.,
Neal M.J.
Publication year - 1990
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1990.tb14644.x
Subject(s) - diazepam , aminobutyric acid , endocrinology , medicine , hippocampal formation , gamma aminobutyric acid , chemistry , pharmacology , receptor
The effects of chronic diazepam administration to rats on the central release of [ 3 H]‐5‐hydroxytryptamine ([ 3 H]‐5‐HT) and [ 14 C]‐γ‐aminobutyric acid ([ 14 C]‐GABA, ex vivo ) were examined. Chronic (5 and 21 days) administration of diazepam (4 mg kg −1 i.p. daily for 21 days) reduced the K‐evoked (20 m m KCl) release of [ 3 H]‐5‐HT from frontal cortex by approximately 50%. Remarkably, this decrease was still present 1 week after diazepam withdrawal. Chronic diazepam treatment did not significantly affect hippocampal [ 3 H]‐5‐HT release but after 21 days the K‐evoked release of [ 14 C]‐GABA was more than doubled and remained elevated 30 h after withdrawal; it returned to control levels after 1 week, and decreased below control levels after 2 weeks. This study indicates that chronic diazepam treatment produces striking changes in transmitter release in rats that persist long after treatment has ceased.

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