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EEG effects of buspirone and pindolol: A method of examining 5-HT1A receptor function in humans

Lookup NU author(s): Professor Hamish McAllister-WilliamsORCiD, Dr Alice Massey


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Rationale: An involvement of 5-HT1A receptors is postulated in the pathophysiology of affective disorders and mechanism of action of antidepressants. Methods for studying their functional integrity in humans are, however, limited. Preliminary data suggests that activation of somatodendritic 5-HT1A receptors cause a negative shift in the EEG frequency spectrum. Animal research suggests that pindolol is an agonist at these receptors but an antagonist at postsynaptic 5-HT1A receptors. Objective: We postulated that while pindolol would antagonise known postsynaptic mediated neuroendocrine responses to the 5-HT1A agonist buspirone, both drugs would have a similar effect on the EEG frequency spectrum. Methods: Fourteen healthy men were administered placebo or pindolol (20 mg orally) 90 min before placebo or buspirone (30 mg orally) in a double blind cross-over study. Plasma prolactin and growth hormone were assayed and EEGs recorded before and after drug administration. Results: A significant negative shift in the EEG frequency spectrum was found for both buspirone and pindolol, with the combination producing a similar effect to each drug alone. In contrast, the neuroendocrine response to buspirone was significantly attenuated by pindolol. Conclusions: The data obtained are consistent with the EEG effects of buspirone and pindolol being mediated by somatodendritic 5-HT1A receptors, in contrast to the neuroendocrine response, which is known to be mediated by postsynaptic receptors. The development of this novel method of assessing somatodendritic 5-HT1A receptors in humans is a potentially important advance which may allow the testing of hypotheses of its involvement in depression and response to antidepressants.

Publication metadata

Author(s): McAllister-Williams RH, Massey AE

Publication type: Article

Publication status: Published

Journal: Psychopharmacology

Year: 2003

Volume: 166

Issue: 3

Pages: 284-293

Print publication date: 01/03/2003

ISSN (print): 0033-3158

ISSN (electronic): 1432-2072

Publisher: Springer

PubMed id: 12589521