The excitability of relay neurons in the dorsal geniculate nucleus (dLGN) can be altered by a variety of neuromodulators. The dLGN receives substantial dopaminergic input from the brainstem and this innervation may play a crucial role in the gating of visual information from the retina to visual neocortex. In this study, we investigated the action of dopamine on identified dLGN neurons using whole cell recording techniques. Dopamine (2-200 µM) produced a membrane depolarization in >95% of relay neurons tested, but did not alter excitability of dLGN interneurons. The D1-like dopamine receptor agonist SKF38393 (2-50 µM) produced a similar depolarization in dLGN relay neurons. However, the D2-like receptor agonists, bromocriptine (25-50 µM) and PPHT (1-50 µM), did not alter the membrane potential of relay neurons. SCH23390 (5-10 µM), a D1-like receptor antagonist, attenuated the depolarizing actions of both dopamine and SKF38393. Furthermore, the excitatory actions of dopamine and SKF38393 were attenuated by ZD7288, a specific antagonist for the hyperpolarization activated mixed cation current, I_h. Our data suggest that dopamine, acting via D1-like receptors, activates I_h leading to a membrane depolarization. Through the modulation of dLGN neuronal excitability, ascending and descending activating systems may not only control the state of the thalamus such as the transition from slow-wave sleep to waking, but also regulate the efficacy of information transfer during waking states.