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Nicotine regulates 5‐HT 1A receptor gene expression in the cerebral cortex and dorsal hippocampus
Author(s) -
Kenny Paul J.,
File Sandra E.,
Rattray Marcus
Publication year - 2001
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.0953-816x.2001.01501.x
Subject(s) - nicotine , dentate gyrus , hippocampus , medicine , endocrinology , cerebral cortex , receptor , in situ hybridization , central nervous system , chemistry , biology , neuroscience , gene expression , gene , biochemistry
The 5‐HT 1A receptor has previously been shown to be important in mediating the behavioural effects of nicotine. It is possible that nicotine administration might regulate the levels of 5‐HT receptors in limbic and cortical regions, and such regulations may underlie adaptive responses to nicotine in the central nervous system. The effects of acute and chronic systemic (–)‐nicotine administration on 5‐HT 1A receptor gene expression were measured by in situ hybridization, in the rat cerebral cortex, dorsal hippocampus and lateral septum. In the cortex, acute nicotine (0.5 mg/kg i.p.) significantly increased the expression of 5‐HT 1A receptor mRNA 2 h and 24 h after injection. Similarly, acute nicotine significantly increased 5‐HT 1A receptor mRNA in the dentate gyrus (DG), CA3 and CA1 regions of the dorsal hippocampus 2 h and 24 h after injection. Acute nicotine was without effect in the lateral septum. Chronic nicotine (0.5 mg/kg i.p; twice daily for 7 days) significantly decreased 5‐HT 1A receptor mRNA in the cortex 2 h after the final injection, but was without effect at 24 h or 72 h. Chronic nicotine caused no changes in 5‐HT 1A mRNA in the lateral septum or dorsal hippocampus. These data demonstrate that nicotine regulates 5‐HT 1A receptor gene expression in the cortex and hippocampus. The rapid regulation of expression of 5‐HT 1A receptor mRNA leads to the hypothesis that nicotine‐induced 5‐HT release may alter the postsynaptic sensitivity to 5‐HT.