Dopamine enhances the excitability of somatosensory thalamocortical neurons.

The thalamus conveys sensory information from peripheral and subcortical regions to the neocortex in a dynamic manner that can be influenced by several neuromodulators. Alterations in dopamine (DA) receptor function in thalami of Schizophrenic patients have recently been reported. In addition, schizophrenia is associated with sensory gating abnormalities and sleep-wake disturbances, thus we examined the role of DA on neuronal excitability in somatosensory thalamus. The ventrobasal (VB) thalamus receives dopaminergic innervation and expresses DA receptors; however, the action of DA on VB neurons is unknown. In the present study, we performed whole cell current- and voltage-clamp recordings in rat brain slices to investigate the role of DA on excitability of VB neurons. We found that DA increased action potential discharge and elicited membrane depolarization via activation of different receptor subtypes. Activation of D2-like receptors (D(2R)) leads to enhanced action potential discharge, whereas the membrane depolarization was mediated by D1-like receptors (D(1R)). The D(2R-mediated) increase in spike discharge was mimicked and occluded by α-dendrotoxin (α-DTX), indicating the involvement of a slowly inactivating K(+) channels. The D1R-mediated membrane depolarization was occluded by barium, suggesting the involvement of a G protein-coupled K(+) channel or an inwardly rectifying K(+) channel. Our results indicate that DA produces dual modulatory effects acting on subtypes of DA receptors in thalamocortical relay neurons, and likely plays a significant role in the modulation of sensory information.