Suppression of haloperidol-induced oral dyskinesias in rats by vigabatrin.
Acute and chronic administration of vigabatrin, a selective inactivator of GABA-T, suppresses haloperidol-induced dyskinesias at low doses without preventing the enhancement of striatal dopamine D2 receptor density or the development of vacuous chewing movements. The long-term administration of vigabatrin does not attenuate its effect. The observations presented in this work support the GABA hypothesis of haloperidol-induced vacuous chewing behavior in rats, and suggest that vigabatrin is an appropriate means to enhance nigral GABAergic activity.
Seiler
N
N
Marion Merrel Dow Research Institute, Strasbourg, France.
Grauffel
C
C
Elands
J
J
van den Buuse
M
M
Knödgen
B
B
Sarhan
S
S
Moran
P
P
Gobaille
S
S
D000612:4-Aminobutyrate Transaminase / Q000378:metabolism; D000818:Animals; D000927:Anticonvulsants / Q000493:pharmacokinetics / Q000627:therapeutic use*; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000473:pathology; D004409:Dyskinesia, Drug-Induced / Q000473:pathology / Q000517:prevention & control*; D004435:Eating / Q000187:drug effects; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006220:Haloperidol / Q000037:antagonists & inhibitors* / Q000633:toxicity; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D017448:Receptors, Dopamine D2 / Q000378:metabolism; D013239:Stereotyped Behavior / Q000187:drug effects; D013469:Sulpiride / Q000494:pharmacology; D020888:Vigabatrin; D005680:gamma-Aminobutyric Acid / Q000031:analogs & derivatives* / Q000378:metabolism / Q000493:pharmacokinetics / Q000627:therapeutic use
D000927:Anticonvulsants; D017448:Receptors, Dopamine D2; D005680:gamma-Aminobutyric Acid; D013469:Sulpiride; D000612:4-Aminobutyrate Transaminase; D005968:Glutamate Decarboxylase; D020888:Vigabatrin; D006220:Haloperidol