JPET Introducing ALZET?ew Model 2006 Pump

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
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 Masonis, A. E.
Right arrow Articles by McCarthy, M. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Masonis, A. E.
Right arrow Articles by McCarthy, M. P.

Effects of the androgenic/anabolic steroid stanozolol on GABAA receptor function: GABA-stimulated 36Cl- influx and [35S] TBPS binding

AE Masonis and MP McCarthy

Dept. of Pharmacology, UMDNJ-Robert Wood Johnson Medical School, Piscataway.

We have recently demonstrated that androgenic/anabolic steroids modulate in vitro ligand binding to the benzodiazepine binding site(s) associated with the gamma-aminobutyric acidA (GABAA) receptor complex (Masonis and McCarthy, 1995). One androgenic/anabolic steroid in particular, stanozolol, appears to stabilize the GABAA receptor in a moderate-affinity state for benzodiazepine binding. In the present study, we demonstrate the effects of stanozolol on the functional responsiveness of the GABAA receptor. After pre-incubation with stanozolol, we observed a decrease in the Emax and EC50 values for GABA- stimulated 36Cl- influx into cortical synaptoneurosomes. Moreover, in the presence of stanozolol, flunitrazepam-enhanced GABA-stimulated 36Cl- influx was lost, and the GABAA receptor was stabilized in a functional state that was resistant to further desensitization by agonist. Stanozolol does not appear to reduce GABA-stimulated 36Cl- influx by acting as a channel blocker at the well-characterized channel blocker binding site, as illustrated by the GABA-sensitive biphasic effects of stanozolol on [35S] t-butylbicyclophosphorothionate binding. These results demonstrate a novel, nongenomic mechanism for androgenic/anabolic steroidal modulation of CNS function.

Volume 279, Issue 1, pp. 186-193, 10/01/1996
Copyright © 1996 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
 Recent Prog Horm ResHome page
C. M. Kuhn
Anabolic Steroids
Recent Prog. Horm. Res., January 1, 2002; 57(1): 411 - 434.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
J. C. Jorge-Rivera, K. L. McIntyre, and L. P. Henderson
Anabolic Steroids Induce Region- and Subunit-Specific Rapid Modulation of GABAA Receptor-Mediated Currents in the Rat Forebrain
J Neurophysiol, June 1, 2000; 83(6): 3299 - 3309.
[Abstract] [Full Text] [PDF]


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

Copyright © 1996 by the American Society for Pharmacology and Experimental Therapeutics.