Dopamine/glutamate interaction as studied by combining turning behaviour and c-Fos expression.

Dopamine (DA) and glutamate N-methyl-D-aspartate (NMDA) receptors extensively interact in the mediation of motor behaviours originated in basal ganglia. In unilaterally 6-hydroxydopamine (6-OHDA) lesioned rats, this interaction is of a different sign depending on whether D1 or D2 receptors are stimulated. Contralateral turning behaviour induced by D1 agonists is potentiated by the NMDA antagonist MK 801, while turning behaviour induced by D2 agonists is decreased. NMDA receptors not only modulate the acute turning behaviour induced by DA agonists but also the long-term effects induced by stimulation of DA receptors. MK 801, in fact, prevents the sensitization (priming) of D1-mediated turning behaviour induced by a single exposure to a DA agonist. Prevention of priming by MK 801, also appears to be different depending on whether D1 or D1/D2 receptors are stimulated. Studies on c-fos expression induced by DA D1 agonists in the 6-OHDA lesioned striatum show that detection of Fos-like immunoreactivity correlates to the long-term but not the acute effects induced by DA receptor stimulation and NMDA receptor blockade.