Dissociation between drug-induced increases in nerve terminal and non-nerve terminal pools of GABA in vivo.
To examine whether increased GABA levels produced by n-dipropylacetate (DPA) and amino-oxyacetic acid (AOAA) are associated with nerve terminals, we compared the effect of these drugs on the GABA content of substantia nigra (SN) in rats in which the GABAergic afferent projections to SN had been unilaterally destroyed. In the SN largely devoid of GABAergic nerve terminals, AOAA (30 mg/kg) produced a 2-fold increase in GABA, whereas DPA (300 mg/kg) was without effect. Since DPA and AOAA both increased GABA to a similar extent in the intact SN, it appears that the GABA increase produced by DPA is associated with GABAergic nerve terminals, while AOAA primarily elevates GABA in non-nerve terminal components (neural perikarya and glial cells) which are not destroyed by our lesions.
D000625:Aminooxyacetic Acid / Q000494:pharmacology; D000818:Animals; D008297:Male; D009411:Nerve Endings / Q000187:drug effects / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000378:metabolism; D051381:Rats; D013378:Substantia Nigra / Q000378:metabolism; D014635:Valproic Acid / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D009419:Nerve Tissue Proteins; D000625:Aminooxyacetic Acid; D005680:gamma-Aminobutyric Acid; D014635:Valproic Acid