Citation

Dewey SL, Chaurasia CS, Chen CE, Volkow ND, Clarkson FA, Porter SP, Straughter-Moore RM, Alexoff DL, Tedeschi D, Russo NB, Fowler JS, Brodie JD. Synapse 1997; 25(4): 393-398.

Copyright

(Copyright © 1997, John Wiley and Sons)

DOI

10.1002/(SICI)1098-2396(199704)25:4<393::AID-SYN11>3.0.CO;2-W

PMID

9097399

Abstract

GABA modulates dopamine concentrations in the nucleus accumbens and corpus striatum. Using in vivo microdialysis techniques we examined this modulatory role and the extent to which three different GABAergic drugs can attenuate cocaine's ability to increase extracellular dopamine concentrations and gross locomotor activity. Ethanol, lorazepam (Ativan), and gamma-vinyl GABA (GVG) significantly and dose-dependently attenuated cocaine-induced dopamine release in the corpus striatum of freely moving animals. Unlike ethanol or lorazepam, however, GVG is not a sedative hypnotic in the doses used, and hence the strategy of selectively increasing GABAergic activity by suicide inhibition of the catabolic enzyme, GABA-transaminase, offers the unique advantage of attenuating cocaine-induced dopamine release without the apparent side effects typically associated with sedative hypnotics.

Language: en

Keywords

4-Aminobutyrate Transaminase; Animals; Cocaine; Corpus Striatum; Dopamine; Enzyme Inhibitors; Ethanol; GABA Modulators; gamma-Aminobutyric Acid; Lorazepam; Male; Microdialysis; Motor Activity; Rats; Rats, Sprague-Dawley; Time Factors; Vigabatrin