Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow E-Letters: Submit a response to the article
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (12)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Schulte, D.
Right arrow Articles by Stamford, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schulte, D.
Right arrow Articles by Stamford, J. A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

British Journal of Anaesthesia, Vol 84, Issue 2 250-253, Copyright © 2000 by Oxford University Press

ARTICLES

Propofol decreases stimulated dopamine release in the rat nucleus accumbens by a mechanism independent of dopamine D2, GABAA and NMDA receptors

D Schulte, LF Callado, C Davidson, PE Phillips, N Roewer, J Schulte am Esch and JA Stamford
Department of Anaesthesiology, University Hospital Eppendorf, Hamburg, Germany.

Although propofol (2,6-di-isopropylphenol) is a popular i.v. general anaesthetic, it has been suggested to have abuse potential. As many drugs of abuse act preferentially via release of dopamine in the limbic system, we investigated the action of propofol on stimulated dopamine release in the rat nucleus accumbens. Nucleus accumbens slices were superfused (1.6 ml min-1) with artificial cerebrospinal fluid at 32 degrees C. Dopamine release was evoked by electrical stimulation (10 pulses, 0.1 ms, 10 mA, 10 Hz, every 10 min) and monitored by fast cyclic voltammetry. Propofol 100 mumol litre-1 reduced stimulated dopamine release over the 2 h after administration, relative to intralipid controls, to mean 30 (SEM 2)% (P < 0.01). The dopamine D2 receptor antagonist metoclopramide 0.3 mumol litre-1 increased dopamine release but did not block the effect of propofol (38 (3)%). The selective GABAA antagonist bicuculline 24 mumol litre-1 also failed to antagonize the action of propofol (45 (3)%). The NMDA receptor antagonist dextromethorphan 10 mumol litre-1 decreased dopamine release to 57 (6)% (P < 0.01) but failed to block the inhibitory effect of propofol (46 (6)%). Although propofol has been reported to bind to D2, GABAA and NMDA receptors, failure of metoclopramide and bicuculline to block its effects suggests that an agonist action at D2 or GABAA receptors does not mediate the effects of propofol on dopamine release in the rat nucleus accumbens. The lack of effect of dextromethorphan makes an NMDA receptor antagonist action unlikely.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Pharmacol. Exp. Ther.Home page
K.-Y. Li, C. Xiao, M. Xiong, E. Delphin, and J.-H. Ye
Nanomolar Propofol Stimulates Glutamate Transmission to Dopamine Neurons: A Possible Mechanism of Abuse Potential?
J. Pharmacol. Exp. Ther., April 1, 2008; 325(1): 165 - 174.
[Abstract] [Full Text] [PDF]

Home page
 Br J AnaesthHome page
J. A. Gredell, P. A. Turnquist, M. B. MacIver, and R. A. Pearce
Determination of diffusion and partition coefficients of propofol in rat brain tissue: implications for studies of drug action in vitro
Br. J. Anaesth., December 1, 2004; 93(6): 810 - 817.
[Abstract] [Full Text] [PDF]

Home page
 Anesth. Analg.Home page
L. Pain, S. Gobaille, C. Schleef, D. Aunis, and P. Oberling
In Vivo Dopamine Measurements in the Nucleus Accumbens After Nonanesthetic and Anesthetic Doses of Propofol in Rats
Anesth. Analg., October 1, 2002; 95(4): 915 - 919.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.