The thalamic midline paraventricular nucleus (PVT) is prominently innervated by vasopressin-immunoreactive neurons from the suprachiasmatic nucleus (SCN), site of the brain's biological clock. Using patch-clamp recordings in slice preparations taken from Wistar rats during the subjective day, we examined 90 PVT neurons for responses to bath-applied arginine-vasopressin (AVP, 0.5 - 2µM; 1-3 min). In current clamp at resting membrane potentials (-65 ± 1 mV), PVT neurons displayed low threshold spikes (LTSs) and burst firing patterns. In 50% of cells tested, AVP induced a slowly rising, prolonged membrane depolarization and tonic firing, returning to burst firing upon recovery. AVP modulated hyperpolarization-activated LTSs by decreasing the time to the initial sodium spike at the onset of LTS, also increasing the duration of the afterdepolarization. Responses were blockable with a V_1a receptor antagonist (Manning compound). Under voltage-clamp, AVP-induced a tetrodotoxin-resistant, slowly rising and prolonged (~ 15 minutes) inward current (<40 pA). I-V analyses of the AVP responses revealed a decrease in membrane conductance to 73.1 ± 6.2 % of control, with net AVP current reversing at -106 ± 4 mV, and decreased inward rectification at negative potentials. These observations are consistent with an AVP-induced closure of an inwardly rectifying potassium conductance. Based on these in-vitro observations, we suggest that the SCN vasopressinergic innervation of PVT is excitatory in nature, possibly releasing AVP with circadian rhythmicity and contributing to state-dependent firing patterns in PVT neurons over the sleep-wake cycle.