THE purpose of this study was to examine the effects of blockade (sulp
iride) and activation (quinpirole) of dopaminergic D2 (DA2) receptors
on brain lesions subsequent to excessive activation of glutamate (GLU)
receptors. Striatal lesions were produced by direct injection of quin
olinic acid, an endogenous GLU receptor agonist. Sulpiride (100 mg kg-
1 i.p., 30 min before quinolinic acid injection and 1 h after) signifi
cantly (p less-than-or-equal-to 0.05) reduced the volume of the lesion
by around 20%. Quinpirole (1.25 mg kg-1 i.p., 30 min before quinolini
c acid injection) had no effect. The protective action of DA2 receptor
blockade strongly suggests that quinolinic acid-induced excitotoxicit
y may be partly modulated by DA2 receptors.