T. Akasu et S. Shoji, CAMP-DEPENDENT INWARD RECTIFIER CURRENT IN NEURONS OF THE RAT SUPRACHIASMATIC NUCLEUS, Pflugers Archiv, 429(1), 1994, pp. 117-125
Electrophysiological properties of the inward rectification of neurons
in the rat suprachiasmatic nucleus (SCN) were examined by using the s
ingle-electrode voltage-clamp method, in vitro. Inward rectifier curre
nt (I-H) was produced by hyperpolarizing step command potentials to me
mbrane potentials negative to approximately -60 mV in nominally zero-C
a2+ Krebs solution containing tetrodotoxin (1 mu M), tetraethylammoniu
m (40 mM), Cd2+ (500 mu M) and 4-aminopyridine (1 mM). I-H developed d
uring 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 conducta
nce (G(H)) ranged between -55 and -120 mV. The G(H) was 80-150 pS (n=4
) at the half-activation voltage of -84+/-7 mV (n=4). The reversal pot
ential of I-H obtained by instantaneous current voltage (I/V) relation
s was -41+/-6 mV (n=4); it shifted to -51+/-8 mV (n=3) in low-Na+ (20
mM) solution and to -24+/-4 mV (n=4) in high-K+ (20 mM) solution. Fors
kolin (1-10 mu M) produced an inward current and increased the amplitu
de of I-H. Forskolin did not change the half-activation voltage of G(H
). 8-Bromo-adenosine 3',5'-cyclic monophosphate (8-Br-cAMP, 0.1-1 mM)
and dibutyryl-cAMP (0.1-1 mM) enhanced I-H. 3-Isobutyl-1-methylxanthin
e (IBMX, 1 mM) also enhanced I-H. The results suggest that the inward
rectifier cation current is regulated by the basal activity of adenyla
te cyclase in neurons of the rat SCN.