Augmentation of glutamate responses by GABA in the rat's motorcortex in vivo.
The influence of the inhibitory transmitter gamma-aminobutyric acid (GABA) on cortical field potential changes (CFPs) elicited by the excitatory transmitter glutamate and its subreceptor agonists N-methyl-D-aspartate (NMDA) and quisqualate was tested in the motorcortex of anesthetized and artificially ventilated rats. Drugs were applied through a 3-barrelled micropipette by ionophoresis or pressure ejection. Glutamate and its agonists evoked negative and GABA positive CFPs. Applications of GABA before (up to 300 s) the ejection of glutamate, NMDA or quisqualate increased the amplitude of the negative CFP induced by the excitatory transmitters. This augmentation was more pronounced with NMDA and quisqualate than with glutamate. It could be mimicked by the GABAA-agonist muscimol but not by the GABAB-agonist baclofen. It is suggested that the enhancement of glutamate responses by GABA may be mediated by an intracellular common pathway.
Walden
J
J
Institut für Physiologie, Universität Münster, F.R.G.
Speckmann
E J
EJ
Bingmann
D
D
D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D001418:Baclofen / Q000494:pharmacology; D005071:Evoked Potentials / Q000187:drug effects; D005971:Glutamates / Q000494:pharmacology*; D009044:Motor Cortex / Q000187:drug effects / Q000502:physiology*; D009118:Muscimol / Q000494:pharmacology; D016202:N-Methylaspartate; D010069:Oxadiazoles / Q000494:pharmacology; D016318:Quisqualic Acid; D051381:Rats; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D005971:Glutamates; D010069:Oxadiazoles; D009118:Muscimol; D001224:Aspartic Acid; D005680:gamma-Aminobutyric Acid; D016202:N-Methylaspartate; D016318:Quisqualic Acid; D001418:Baclofen