Adrenergic and Serotonergic Receptor Responsiveness in Depression

  1. Ruth Porter Organizer,
  2. Gregory Bock Organizer and
  3. Sarah Clark
  1. Larry J. Siever1,2,
  2. Emil F. Coccaro1,2,
  3. Eric Benjamin2,
  4. Karen Rubinstein1 and
  5. Kenneth L. Davis1,2

Published Online: 28 SEP 2007

DOI: 10.1002/9780470513361.ch9

Ciba Foundation Symposium 123 - Antidepressants and Receptor Function

Ciba Foundation Symposium 123 - Antidepressants and Receptor Function

How to Cite

Siever, L. J., Coccaro, E. F., Benjamin, E., Rubinstein, K. and Davis, K. L. (2007) Adrenergic and Serotonergic Receptor Responsiveness in Depression, in Ciba Foundation Symposium 123 - Antidepressants and Receptor Function (eds R. Porter, G. Bock and S. Clark), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470513361.ch9

Author Information

  1. 1

    Department of Psychiatry, Bronx VA Medical Center, 130 West Knightsbridge Road, Bronx, New York 10468, USA

  2. 2

    Mount Sinai School of Medicine, 1 Gustav Levy Place, New York 10029, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471910893

Online ISBN: 9780470513361

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Keywords:

  • adrenergic receptor;
  • serotonergic receptor;
  • depression;
  • adrenoceptor responsiveness;
  • prolactin responses

Summary

Preliminary results are presented from a series of studies designed to characterize the regulation of release/metabolism and receptor responsiveness in the noradrenergic and serotonergic systems in acutely depressed patients and depressed patients in remission. Abnormal regulation of noradrenaline release/ metabolism might be expected to be associated with the acute state of depression, while abnormalities of adrenoceptor responsiveness were hypothesized to persist in remission. Growth hormone responses to clonidine were measured as indices partially reflecting α2-adrenoceptor responsiveness. Blunted responses to clonidine were found in both acutely depressed patients and patients in remission. The possible implications of these findings for the pathophysiology of the noradrenergic system in depression are discussed.

Prolactin responses to the serotonergic agonist and serotonin-releasing agent fenfluramine were evaluated in acutely depressed patients, patients in remission and controls. A subset of the depressed patients appeared to have blunted prolactin responses to fenfluramine. However, very preliminary results do not show any difference in this response between patients who were acutely ill and those in remission, although the variability in both groups was great. These and related findings are discussed in terms of a possible contributory role of the serotonergic system in depression.