GABA-mediated responses are not selectively depressed by 3-mercaptopropionic acid in the spinal cord.
The competitive inhibitor of glutamic acid decarboxylase (GAD), 3-mercaptopropionic acid (MPA), causes depletion of gamma-aminobutyric acid and convulsions. We expected it to be a superior GABA depleting agent for in vivo experiments to the frequently used semicarbazide. The dorsal root potentials (DRP) and monosynaptic reflex responses (MSR) evoked by adjacent dorsal root and peripheral nerve stimulation, respectively, were recorded in spinal unanaesthetized cats. MPA (100-200 mg/kg) caused a gradual decrease in DRP, reaching a peak in about 40 min after drug administration. This was usually associated with convulsive activity. Postsynaptic direct inhibition was not substantially affected. However, the MSR was consistently decreased, within 10 min after injection of MPA. It is concluded that MPA is not a suitable tool, at least in the spinal cord, for the selective reduction of GABAergic transmission.
D015097:3-Mercaptopropionic Acid / Q000494:pharmacology*; D000818:Animals; D002415:Cats; D005071:Evoked Potentials / Q000187:drug effects; D005260:Female; D018756:GABA Antagonists; D008297:Male; D012023:Reflex, Monosynaptic / Q000187:drug effects; D013116:Spinal Cord / Q000187:drug effects*; D013438:Sulfhydryl Compounds; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018756:GABA Antagonists; D013438:Sulfhydryl Compounds; D005680:gamma-Aminobutyric Acid; D015097:3-Mercaptopropionic Acid