GABAA receptors in the midbrain central grey mediate the antiaversive action of GABA.
Intracerebral injection of the GABAA agonists muscimol (1 nmol), isoguvacine (1 nmol) or THIP (1, 2 and 4 nmol) in rats with chemitrodes implanted in the dorsal midbrain central grey raised the threshold electrical current for inducing escape behaviour. The effect of THIP was dose-dependent. In contrast, the GABAB agonist baclofen (10 and 100 nmol) did not affect the aversive threshold. Furthermore, pretreatment with baclofen (10 nmol and 100 nmol) did not significantly change the effect of THIP (2 nmol). These results indicate that the antiaversive action of GABA in the midbrain central grey is mediated by GABAA but not by GABAB receptors.
D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects*; D001418:Baclofen / Q000494:pharmacology; D004567:Electrodes, Implanted; D007555:Isoxazoles / Q000494:pharmacology; D008297:Male; D008636:Mesencephalon / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011963:Receptors, GABA-A / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D007555:Isoxazoles; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D001418:Baclofen; C015542:gaboxadol