Mechanisms of Excitatory Amino Acid-Induced Stimulation of GABAergic Synaptic Activity in Cultures from the Rat Superior Colliculus

Presynaptic autoreceptors appear to be a ubiquitous regulatory device in many systems (Starke, 1981; Middlemiss, 1988). It is therefore not too surprising that excitatory amino acid receptors (EAARs) have been found on EAA-releasing terminals (Ferkany et al., 1982; Collins et al., 1983; Ferkany and Coyle, 1983; Potashner and Gerard, 1983; Poli et al., 1985) or putative glutamatergic axons (Evans, 1980; Curtis et al., 1984) and terminals (Foster et al., 1981; Represa et al. 1987). More controversial is the notion that EAARs can also modulate the release of the inhibitory neurotransmitter GABA (Pearce and Dutton, 1982; Drejer et al., 1987; Gallo et al., 1987; Harris and Miller, 1989; Pin and Bockaert, 1989). Considering the major role that GABAergic inhibition plays in primary visual brain structures it seems important to further explore the possibility that EAARs participate in the regulation of GABA release. In particular, it should be clarified whether the EAA-stimulated release of GABA is indeed related to the generation of GABAergic synaptic activity. If so, it would be important to localize the respective EAARs and to characterize these EAARs on the basis of the EAA-induced conductance changes.