The role of the glutamate 'metabotropic' receptor was investigated in an experimental model of focal ischaemia-induced neurodegeneration. The metabotropic agonist, trans-1-amino cyclopentane-1,3-dicarboxylic acid (t-ACPD, 20 mg/kg i.p.), was administered to mice immediately after middle cerebral artery occlusion (MCAO), which causes cerebral infarct. Seven days after MCAO, the mean infarct volume value of the t-ACPD-treated group (mean +/- S.E. = 4.57 +/- 0.73 mm3) was significantly reduced, by 34.3%, compared to the vehicle-treated group (mean +/- S.E. = 6.95 +/- 0.59 mm3, P < 0.01). This suggests that metabotropic receptor activation in the adult brain reduces excitotoxicity.