Although dopamine (DA) usually inhibits firing of rat striatal neurons in vivo, iontophoresis of DA with low ejection currents can also potentiate glutamate-evoked activity. We used extracellular single cell recording to examine the DA receptor subtypes involved in such potentiation. At low iontophoretic currents (1-8 nA), both the DA D1 class receptor agonist SKF 38393 and the DA D2 class receptor agonist quinpirole mimicked the ability of DA to facilitate glutamate-induced activity. Acute depletion of DA abolished the excitatory modulation produced by either D1 or D2 agonists but not by DA. Co-administration of SKF 38393 and quinpirole restored the facilitation of glutamate effects in DA-depleted rats. Stimulation of both D1 and D2 class receptors appears to be required for DA to enhance glutamate-induced firing of striatal neurons.