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Potentiation of GABA by Midazolam and Its Therapeutic Effect against Status Epilepticus
Author(s) -
Kaneko Sunao,
Kurahashi Kozo,
Fujita Seiichi,
Fukushima Yutaka,
Sato Tokijiro,
Hill Raymond G.
Publication year - 1983
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1111/j.1440-1819.1983.tb00338.x
Subject(s) - midazolam , status epilepticus , pharmacology , diazepam , anesthesia , anticonvulsant , glutamate receptor , long term potentiation , medicine , chemistry , epilepsy , sedation , receptor , psychiatry
The anticonvulsive effect of midazolam was studied in rats and mice brains. Microiontophoretically applied midazolam (0.2M, pH 3.5) potentiated the GABA effect at the single neurone level, and inhibited neuronal firing in the rat cuneate neurones. Midazolam administered intraperitoneally (15 mg/kg) increased the primary afferent depolarization for at least two hours. Three mg/kg of midazolam slightly increased the glutamate decarboxylase activities in the mice cerebrum and the increase was statistically significant (p < 0.05). The authors reported a case of clinical application of midazolam: a status epilepticus was successfully treated with it, while intravenous diazepam of 30 mg failed to control the status.