Repeated cocaine exposure inhibits the adrenocorticotropic hormone response to the serotonin releaser d-fenfluramine and the 5-HT1A agonist, 8-OH-DPAT
| Autor: | Qian Li, L.D. Van de Kar, Andrew D. Levy |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Male
Agonist Serotonin medicine.medical_specialty medicine.drug_class Fenfluramine Radioimmunoassay Adrenocorticotropic hormone Pharmacology Serotonergic Rats Sprague-Dawley Cellular and Molecular Neuroscience chemistry.chemical_compound Adrenocorticotropic Hormone Cocaine Fluoxetine Internal medicine Renin medicine Animals 5-HT receptor 8-Hydroxy-2-(di-n-propylamino)tetralin 8-OH-DPAT business.industry Prolactin Rats Serotonin Receptor Agonists Endocrinology chemistry Receptors Serotonin Synapses business medicine.drug |
| Zdroj: | Neuropharmacology. 33:335-342 |
| ISSN: | 0028-3908 |
| DOI: | 10.1016/0028-3908(94)90063-9 |
| Popis: | The influence of cocaine exposure on serotonergic neurons and postsynaptic 5-HT 1A receptor-mediated responses was evaluated by measuring neuroendocrine responses to a serotonin (5-HT) releaser or a 5-HT 1A agonist. Male rats received cocaine (15 mg/kg, i.p.) or saline twice daily for 7 days. Forty-two hr after the final cocaine injection, the 5-HT releaser d-fenfluramine (0, 0.2, 0.6, 2, or 5 mg/kg, i.p.) or the 5-HT 1A agonist, 8-OH-DPAT (0, 10, 50, 200 or 500 μg/kg, s.c.) were administered. Blood samples were then collected for analysis of plasma ACTH, prolactin, and renin concentrations. The ACTH responses to d-fenfluramine and 8-OH-DPAT were inhibited in cocaine pretreated rats. However, the prolactin responses to d-fenfluramine and 8-OH-DPAT were not significantly modified by cocaine exposure. Additionally, the renin response to d-fenfluramine was unaltered by repeated cocaine administration, while 8-OH-DPAT did not alter renin secretion in either pretreatment group. In contrast to published reports which show that cocaine exposure produces supersensitive 5-HT 2A and/or 5-HT 2C receptor-mediated responses, the present data suggest that repeated cocaine exposure produces subsensitivity to at least some postsynaptic 5-HT 1A receptors. Cocaine-induced deficits in the ACTH response to 5-HT releasers may reflect 5-HT 1A receptor subsensitivity, but presynaptic deficits cannot be excluded. Examination of the ACTH response to 5-HT 1A agonists may represent a valuable approach to deermine deficits in 5-HT function in human cocaine abusers. |
| Databáze: | OpenAIRE |
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