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Author Notes:

Corresponding Author and Reprint Requests: Jay M. Weiss, Ph.D., Emory University School of Medicine, Emory West Campus, Building A, Room 510-N, 1256 Briarcliff Road, N.E., Atlanta, GA 30306, Telephone: 404-712-9771, Fax: 404-712-9755, jweis01@emory.edu

Subjects:

Research Funding:

Public Health Service Grants MH65737 and MH79794

Keywords:

  • antidepressant drug
  • electroconvulsive shock
  • dopamine
  • ventral tegmentum

EFFECTS OF CHRONIC ANTIDEPRESSANT DRUG ADMINISTRATION AND ELECTROCONVULSIVE SHOCK ON ACTIVITY OF DOPAMINERGIC NEURONS IN THE VENTRAL TEGMENTUM

Tools:

Journal Title:

International Journal of Neuropsychopharmacology

Volume:

Volume 14, Number 2

Publisher:

, Pages 201-210

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Increasing attention is now focused on reduced dopaminergic neurotransmission in the forebrain as participating in depression. The present paper assessed whether effective antidepressant (AD) treatments might counteract, or compensate for, such a change by altering the neuronal activity of dopaminergic neurons in the ventral tegmental area (VTA-DA neurons), the cell bodies of the mesocorticolimbic dopaminergic system. Eight AD drugs or vehicle were administered to rats for 14 days via subcutaneously-implanted minipumps, at which time single-unit electrophysiological activity of VTA-DA neurons was recorded under anesthesia. Also, animals received a series of five electroconvulsive shocks (ECS) or control procedures, after which VTA-DA activity was measured either three or five days after the last ECS. Results showed that the chronic administration of all AD drugs tested except for the monoamine oxidase inhibitor increased the spontaneous firing rate of VTA-DA neurons, while effects on “burst” firing activity were found to be considerably less notable or consistent. ECS increased both spontaneous firing rate and burst firing of VTA-DA neurons. It is suggested that the effects observed are consistent with reports of increased dopamine release in regions to which VTA neurons project after effective AD treatment. However, it is further suggested that changes in VTA-DA neuronal activity in response to AD treatment should be most appropriately assessed under conditions associated with depression, such as stressful conditions.

Copyright information:

© Cambridge University Press 2014

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