FOS and JUN as markers for ethanol-sensitive pathways in the rat brain

• Published in: Brain research bulletin Vol. 39; no. 3; pp. 177 - 184
• Main Authors: Davidson, M., Matsumoto, I., Shanley, B.C., Wilce, P.A.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 1996; Elsevier Science
• Subjects: Alcoholism and acute alcohol poisoning; Animals; Biological and medical sciences; Brain - drug effects; Cerebral cortex; Cerebral Cortex - drug effects; Dose-Response Relationship, Drug; Ethanol; Ethanol - pharmacology; Genes, jun - drug effects; Hippocampus; Hippocampus - drug effects; Immediate early gene; Male; Medical sciences; N-methyl- d-aspartate; Neural Pathways - drug effects; Proto-Oncogene Proteins c-fos - metabolism; Rats; Rats, Wistar; Toxicology; γ-aminobutyric acid; Cerebral cortex; Ethanol; N-methyl- d-aspartate; γ-aminobutyric acid; Hippocampus; Immediate early gene; Rat; Toxicity; Rodentia; Central nervous system; Gene expression; Vertebrata; Sensitivity; Mammalia; Animal; Excitatory aminoacid; GABA; NMDA receptor; Gabaergic receptor A; Brain (vertebrata)
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/0361-9230(95)02091-8

The expression of proteins coded by the immediate early genes of the
fos family and c-
jun was used to study the effect of acute ethanol administration on convulsant-induced neuronal activity in rat brain. Immunoreactivity for both types of protein was induced by either SC injection of pentylenetetrazole or by IP injection of
N-methyl-
d-aspartic acid. Both agents elicited distinct patterns of behaviour and a high level of FOS-immunoreactivity in the cerebral cortex and hippocampus. Acute IP doses of ethanol (1.0–3.0 g/kg) significantly reduced the behaviours and FOS-immunoreactivity induced in the cerebral cortex by both pentylenetetrazole and
N-methyl-
d-aspartic acid. Pentylenetetrazole-induced FOS-immunoreactivity in the hippocampus was also inhibited by ethanol. In contrast,
N-methyl-
d-aspartic acid-induced FOS-immunoreactivity in the hippocampus was not inhibited by any dose of ethanol. c-JUN immunoreactivity showed a distinct pattern of induction in the hippocampus after injection of
N-methyl-
d-aspartic acid. Ethanol (3.0 g/kg) inhibited
N-methyl-
d-aspartic acid-induced c-JUN-immunoreactivity in the hippocampus and cerebral cortex. The differences in inhibition of immunoreactivity suggest that the sensitivity of the NMDA- and GABA
A-related neuronal pathways to ethanol varies among different anatomical structures.