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Cocaine Regulation of Brain Preprothyrotropin‐Releasing Hormone mRNA
Author(s) -
Sevarino Kevin A.,
Primus Renée J.
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb03267.x
Subject(s) - nucleus accumbens , amygdala , hypothalamus , endocrinology , medicine , hippocampus , thalamus , messenger rna , chemistry , biology , central nervous system , neuroscience , biochemistry , gene
Clinical and preclinical evidence supports a possible role for thyrotropin‐releasing hormone (TRH) in cocaine action. However, the interaction between cocaine and TRH has not been directly examined. In the following report we describe a solution hybridization RNase protection assay that can sensitively detect mRNA for the TRH precursor, prepro‐TRH (ppTRH). Using this assay, we examined ppTRH mRNA levels in rat brain regions implicated in cocaine reinforcement, including the nucleus accumbens, hypothalamus, amygdala, hippocampus, and thalamus. Acute cocaine treatment (15 mg/kg) resulted in significant decreases in ppTRH mRNA levels in the amygdala and hippocampus, but not in the hypothalamus, nucleus accumbens, or thalamus, 45 min postinjection. Chronic cocaine treatment (15 mg/kg twice daily for 14 days) resulted in marked regulation in all regions but the thalamus. Regulation was strongly dependent on the length of cocaine withdrawal and persisted up to 72 h postinjection in the amygdala. These studies support the hypothesis that TRH or other ppTRH‐derived peptides are involved in cocaine action, especially in the extrahypothalamic regions of the amygdala and hippocampus.