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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.
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
