cAMP-dependent inward rectifier current in neurons of the rat suprachiasmatic nucleus

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Abstract
Electrophysiological properties of the inward rectification of neurons in the rat suprachiasmatic nucleus (SCN) were examined by using the single-electrode voltage-clamp method, in vitro. Inward rectifier current (I H) was produced by hyperpolarizing step command potentials to membrane potentials negative to approximately −60 mV in nominally zero-Ca2+ Krebs solution containing tetrodotoxin (1 μM), tetraethylammonium (40 mM), Cd2+ (500 μM) and 4-aminopyridine (1 mM).I H developed during the hyperpolarizing step command potential with a duration of up to 5 s showing no inactivation with time.I H was selectively blocked by extracellular Cs+ (1 mM). The activation of the H-channel conductance (G H) ranged between −55 and −120 mV. TheG H was 80–150 pS (n=4) at the half-activation voltage of −84±7 mV (n=4). The reversal potential ofI H obtained by instantaneous current voltage (I/V) relations was −41±6mV (n=4); it shifted to −51±8mV (n=3) in low-Na+ (20 mM) solution and to −24±4 mV (n=4) in high-K+ (20 mM) solution. Forskolin (1–10 μM) produced an inward current and increased the amplitude ofI H. Forskolin did not change the half-activation voltage ofG H. 8-Bromo-adenosine 3′,5′-cyclic monophosphate (8-Br-cAMP, 0.1–1 mM) and dibutyryl-cAMP (0.1–1 mM) enhancedI H. 3-Isobutyl-1-methylxanthine (IBMX, 1 mM) also enhancedI H. The results suggest that the inward rectifier cation current is regulated by the basal activity of adenylate cyclase in neurons of the rat SCN.