JPET

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by BLISS, E. L.
Right arrow Articles by ZWANZIGER, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by BLISS, E. L.
Right arrow Articles by ZWANZIGER, J.
Journal of Pharmacology And Experimental Therapeutics, Vol. 164, Issue 1, 122-134, 1968
Copyright © 1968 by American Society for Pharmacology and Experimental Therapeutics

METABOLISM OF NOREPINEPHRINE, SEROTONIN AND DOPAMINE IN RAT BRAIN WITH STRESS

EUGENE L. BLISS 1, JANIE AILION 1, and JANET ZWANZIGER 1

1 Department of Psychiatry, University of Utah College of Medicine, Salt Lake City, Utah

The stress of foot shock in rats induces large decreases in the level of brain norepinephrine but does not greatly alter the concentration of serotonin or dopamine in brain. These decrements in norepinephrine are not limited to any region and occur uniformly throughout the brain. However, absolute levels of these amines are not a true indicator of their dynamic state. By various techniques it could be demonstrated that the stress of foot shock accelerates the metabolism of dopamine and serotonin to the same degree as norepinephrine; the only difference being that dopamine and serotonin are rapidly resynthesized, whereas norepinephrine in the brain cannot be regenerated at the same rate. Furthermore, the increased catabolism of brain norepinephrine with stress is blocked by monoamine oxidase inhibitors, whereas catechol-O-methyltransferase inhibitors do not impede accelerated degradation.

Submitted on December 11, 1967
Accepted on July 25, 1968




This article has been cited by other articles:


Home page
 J. Neurosci.Home page
N. L. Schramm, M. P. McDonald, and L. E. Limbird
The {alpha}2A-Adrenergic Receptor Plays a Protective Role in Mouse Behavioral Models of Depression and Anxiety
J. Neurosci., July 1, 2001; 21(13): 4875 - 4882.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
L. E. Goldstein, A. M. Rasmusson, B. S. Bunney, and R. H. Roth
Role of the Amygdala in the Coordination of Behavioral, Neuroendocrine, and Prefrontal Cortical Monoamine Responses to Psychological Stress in the Rat
J. Neurosci., August 1, 1996; 16(15): 4787 - 4798.
[Abstract] [Full Text] [PDF]

Home page
 ScienceHome page
R. Becker, C Giambalvo, R. Fox, and M Macho
Endogenous inhibitors of monoamine oxidase present in human cerebrospinal fluid
Science, July 29, 1983; 221(4609): 476 - 478.
[Abstract] [PDF]

Home page
 Arch Gen PsychiatryHome page
A. Frazer, G. N. Pandey, and J. Mendels
Metabolism of Tryptophan in Depressive Disease
Arch Gen Psychiatry, October 1, 1973; 29(4): 528 - 535.
[Abstract] [PDF]

Home page
 ScienceHome page
A. J. Lewy and L. S. Seiden
Operant Behavior Changes Norepinephrine Metabolism in Rat Brain
Science, January 28, 1972; 175(4020): 454 - 456.
[Abstract] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1968 by the American Society for Pharmacology and Experimental Therapeutics.