Abstract
1. Using whole-cell patch-clamp recordings, infrared videomicroscopy and fast focal solution exchange methods, the actions of neuropeptide Y (NPY) were examined in thalamic slices of postnatal (10-16 days) rats. 2. NPY activated a K+-selective current in neurons of the thalamic reticular nucleus (RT; 20/29 neurons) and ventral basal complex (VB; 19/25 neurons). The currents in both nuclei had activation and deactivation kinetics that were very similar to those of GABAB receptor-induced currents, were totally blocked by 0.1 mM Ba2+ and showed voltage-dependent relaxation. These properties indicate that the NPY-sensitive K+ current is mediated by G-protein-activated, inwardly rectifying K+ (GIRK) channels. 3. In RT neurons, NPY application reversibly reduced high-voltage-activated (HVA) currents to 33 +/- 5 % (n = 40) of the control level but did not affect the T-type currents. Inhibition of Ca2+ currents was voltage independent and was largely mediated by effects on N- and P/Q-type channels. 4. NPY activation of GIRK channels was mediated via NPY1 receptors, whereas inhibition of N- and P/Q-type Ca2+ channels was mediated by NPY2 receptors. 5. These results show that neuropeptide Y activates K+ channels and simultaneously inhibits HVA Ca2+ channels via different receptor subtypes.