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Lignocaine–induced convulsion does not induce c–fos protein (c–Fos) in rat hippocampus
Author(s) -
NAKAO S.,
KURATA J.,
ARAI T.,
MURAKAWA M.,
ADACHI T.,
AVRAMOV M. N.,
MORI K.,
YASUHARA O.,
TOOYAMA I.,
KIMURA H.
Publication year - 1994
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1994.tb04016.x
Subject(s) - piriform cortex , neocortex , hippocampus , convulsion , pentylenetetrazol , convulsants , medicine , thalamus , hippocampal formation , c fos , amygdala , cerebral cortex , anesthesia , limbic system , endocrinology , central nervous system , neuroscience , epilepsy , biology , gene expression , anticonvulsant , biochemistry , psychiatry , gene , radiology
Recent studies have shown that proto–oncogene c–fos mRNA is induced in the central nervous system by a variety of stimuli including generalised convulsions. In this study, the expression of c–fos protein (c–Fos) following lignocaine–induced convulsions was examined and compared with that following convulsions induced by non–anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain. Administration of 120 mg kg ‐1 lignocaine by the intraperitoneal route induced generalised convulsions in all rats examined within 10 min. C–Fos was markedly induced in the piriform cortex and amygdala, and slightly induced in the neocortex and thalamus, while no c–Fos expression was observed in the hippocampus. In contrast, c–Fos expression following generalised convulsions induced by non–anaesthetic convulsants was very marked in the hippocampal region, piriform cortex and amygdala, and extended to the thalamus and neocortex. These results contradict those of previously reported local cerebral metabolic studies using 2–deoxyglucose as a metabolic marker, and suggest that lignocaine–induced convulsions, unlike those induced by non–anaesthetic convulsants, may not cause severe sequelae (plastic changes) in the hippocampus.