Activation of quisqualate metabotropic receptors reduces glutamate and GABA-mediated synaptic potentials in the rat striatum.

The role of quisqualate (QUIS) metabotropic receptors in the synaptic transmission in the striatum was investigated using the cortico-striatal slice preparation. Low concentrations (1-30 microM) of trans-1-amino-cyclopentyl-1,3- dicarboxylic acid (t-ACPD), a selective agonist of QUIS metabotropic receptors, decreased glutamate-mediated synaptic potentials (EPSPs) evoked in the striatum by the stimulation of cortico-striatal fibers. This agonist decreased also GABA-mediated depolarizing synaptic potentials evoked by intrastriatal stimulation in the presence of 6-cyano-7-nitro-quinoxaline-2,3- dione (CNQX); this effect was less potent than the action of t-ACPD on glutamate-mediated potentials. Low concentrations of t-ACPD did not affect the intrinsic membrane properties of striatal neurons and their postsynaptic responses to exogenous glutamate and GABA. Higher concentrations (50-100 microM) to t-ACPD caused membrane depolarizations and inward currents in several neurons. Our data suggest that low concentrations of t-ACPD selectively reduce synaptic transmission while higher concentrations of this agonist may cause a direct excitatory action on striatal neurons.