(3H)-muscimol, (3H)-nipecotic acid and (3H)-isoguvacine as autoradiographic markers for GABA neurotransmission.

Retinas from rabbit, goldfish and guinea-pig were exposed to (3H) GABA, (3H)-nipecotic acid and (3H)-isoguvacine either by intravitreal injection in vivo or by incubations in a balanced salt solution and the distribution of radioactivity was then studied with autoradiography. All substances labelled a similar set of presumed amacrine cells. Incubating at 0 degrees C, in 10-(5)M ouabain, or in 10-(3)M GABA inhibited the labelling by (3H)-muscimol whereas bicuculline (10-(4)M), and glycine (10-(3)M) were less efficient blockers. The result is interpreted as a neuronal uptake of (3H)-muscimol rather than as a GABA receptor binding. All the substances except (3H)-isoguvacine also labelled glia to such a degree that neuronal labelling was often disguised in rabbits and goldfish. Glial labelling by muscimol was less pronounced in guinea-pig. (3H)-isoguvacine (tested only in rabbits) gave a strong labelling of cells with the distribution of GABA neurons and only little glial labelling.