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J Neurophysiol 78: 1021-1029, 1997;
0022-3077/97 $5.00
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The Journal of Neurophysiology Vol. 78 No. 2 August 1997, pp. 1021-1029
Copyright ©1997 The American Physiological Society

A-Type K+ Current in Neurons Cultured From Neonatal Rat Hypothalamus and Brain Stem: Modulation by Angiotensin II

Desuo Wang, Colin Sumners, Philip Posner, and Craig H. Gelband

Department of Physiology, University of Florida College of Medicine, Gainesville, Florida 32610

Wang, Desuo, Colin Sumners, Philip Posner, and Craig H. Gelband. A-type K+ current in neurons cultured from neonatal rat hypothalamus and brain stem: modulation by angiotensin II. J. Neurophysiol. 78: 1021-1029, 1997. The regulation of A-type K+ current (IA) and the single channel underlying IA in neonatal rat hypothalamus/brain stem cultured neurons were studied with the use of the patch-clamp technique. IA had a threshold of activation between -30 and -25 mV (n = 14). Steady-state inactivation of IA occurred between -80 and -70 mV and had a membrane voltage at which IA was half-maximum of -52.2 mV (n = 14). The mean values for the activation and inactivation (decay) time constants during a voltage step to +20 mV were 2.1 ± 0.3 (SE) ms (n = 8) and 13.6 ± 1.9 ms (n = 8), respectively. Single-channel recordings from outside-out patches revealed A-type K+ channels with voltage-dependent activation, 4-aminopyridine (4-AP) sensitivity, and inactivation kinetics similar to those of IA. The single-channel conductance obtained from cell-attached patches was15.8 ± 1.3 pS (n = 4) in a physiological K+ gradient and 41.2 ± 3.7 pS (n = 5) in symmetrical 140 mM K+. Angiotensin II (Ang II, 100 nM) reduced peak IA by ~20% during a voltage step to +20 mV (n = 8). Similarly, Ang II (100 nM) markedly reduced single A-type K+ channel activity by decreasing open probability (n = 4). The actions of Ang II on IA and single A-type K+ channels were reversible either by addition of the selective angiotensin type 1 (AT1) receptor antagonist losartan (1 µM) or on washout of the peptide. Thus the activation of AT1 receptors inhibits a tetraethylammonium-chloride-resistant, 4-AP-sensitive IA and single A-type K+ channels, and this may underlie some of the actions of Ang II on electrical activity of the brain.




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