Effects of acute dopamine depletion on the electrophysiological properties of striatal neurons

The striatum, the main input nucleus of basal ganglia, receives a massive innervation from the entire cerebral cortex and is in charge of the detection of behaviorally relevant signals. In turn, via its projections to the output nuclei of basal ganglia, the striatum contributes to the organization of appropriate compartmental responses. Substantia nigra pars compacta dopaminergic neurons project predominantly to the striatum and regulate striatal functions. Implications of dopaminergic receptors on the physiology of striatal neurons are now well documented. By contrast, the effects of acute dopamine depletion on striatal neurons remain poorly explored. Here, the α-methyl-para-tyrosine was used to deplete dopamine from rat brain slices. We analyzed the consequences of a α-methyl-para-tyrosine treatment on membrane properties of striatal neurons: the medium-sized spiny neurons and the interneurons (GABAergic, cholinergic and NO-synthase). After acute dopamine depletion, medium-sized spiny neurons became more excitable. GABAergic interneurons became less excitable whereas cholinergic cells displayed an increased excitability. NO-synthase-containing interneurons did not show noticeable changes in their excitability. Such membrane properties changes indicate that striatal circuits should undergo major alteration in cortico-basal ganglia information processing.