IMMUNOHISTOCHEMICAL EVIDENCE FOR FLUPIRTINE ACTING AS AN ANTAGONIST ON THE N-METHYL-D-ASPARTATE AND HOMOCYSTEIC ACID-INDUCED RELEASE OF GABA IN THE RABBIT RETINA
Nn. Osborne et al., IMMUNOHISTOCHEMICAL EVIDENCE FOR FLUPIRTINE ACTING AS AN ANTAGONIST ON THE N-METHYL-D-ASPARTATE AND HOMOCYSTEIC ACID-INDUCED RELEASE OF GABA IN THE RABBIT RETINA, Brain research, 667(2), 1994, pp. 291-294
When rabbit retinas are exposed in vitro to specific excitatory amino
acid receptor agonists certain GABAergic amacrine cells are activated
to cause a release of GABA. The GABA that is not released can be detec
ted by immunohistochemistry. Exposure of tissues to kainate or NMDA ea
ch caused a characteristic change in the GABA immunoreactivity. CNQX a
ntagonised the kainate effect specifically while MK-801 counteracted t
he influence of NMDA The effect produced by kainate was mimicked by do
moic acid while the influence of homocysteic acid was identical with N
MDA. Flupirtine alone did not influence the nature of the GABA immunor
eactivity and so did not act as a kainate or NMDA agonist. However, fl
upirtine counteracted the influence produced by NMDA and homocysteic a
cid but had no effect on the kainate and domoic acid responses. Thus i
n this system flupirtine acts as an NMDA antagonist.