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Long‐term changes in connexin32 gap junction protein and mRNA expression following cocaine self‐administration in rats
Author(s) -
Bennett Steffany A. L.,
Arnold Jennifer M.,
Chen Jiahua,
Stenger Janet,
Paul David L.,
Roberts David C. S.
Publication year - 1999
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.1460-9568.1999.00752.x
Subject(s) - nucleus accumbens , hippocampus , hippocampal formation , in situ hybridization , dopamine , neuroscience , gap junction , messenger rna , biology , chemistry , microbiology and biotechnology , genetics , gene , intracellular
Considerable evidence indicates a critical role for dopamine in the reinforcing effects of cocaine. Because dopamine has been shown to be a critical modulator of gap junction communication in both eye and brain, we sought to examine whether extended intravenous cocaine self‐administration would affect the expression of gap junction channel‐forming proteins (connexins). Using ELISA, Western analysis, immunohistochemistry, semi‐quantitative reverse transcriptase polymerase chain reaction (RT‐PCR), and non‐radioactive in situ hybridization, we demonstrate that withdrawal from chronic cocaine self‐administration causes lasting changes in connexin32 (Cx32) expression in the nucleus accumbens and hippocampus at 2, 7 and 21 days after the last cocaine injection. A sustained decrease in Cx32 protein and mRNA levels is noted in areas that have been implicated in cocaine craving (i.e. nucleus accumbens and subfields of the hippocampal formation). A progressive increase in gap junction protein and mRNA expression is noted in areas that become hyperexcitable after chronic cocaine exposure (i.e. CA1 hippocampal neurons). We speculate that gap junction communication may be critically involved in reinforcement processes and neuroadaptive changes produced by drugs of abuse.