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The Journal of Neurophysiology Vol. 79 No. 3 March 1998,
pp. 1239-1245
Copyright ©1998 The American Physiological Society
1 Istituto di Ricovero e Cura a Carattere Scientifico Santa Lucia, Laboratorio di Neurologia Sperimentale; and 2 Clinica Neurologica, Universita' di Tor Vergata, 00179 Rome, Italy
Guatteo, E., M. Federici, A. Siniscalchi, T. Knöpfel, N. B. Mercuri, and G. Bernardi. Whole cell patch-clamp recordings of rat midbrain dopaminergic neurons isolate a sulphonylurea- and ATP-sensitive component of potassium currents activated by hypoxia. J. Neurophysiol. 79: 1239-1245, 1998. The effects of brief (2-4 min) hypoxia on presumed dopaminergic "principal" neurons of the rat ventral mesencephalon were investigated by using either intracellular or whole cell patch-clamp recordings in in vitro conditions. Under single-electrode voltage clamp, with sharp microelectrode (Vh 
60 mV), a brief hypoxia caused an outward current (hypoOUT) of 110.2 ± 15.2 (SE) pA (n = 18), which was followed by a posthypoxic outward current (posthypoOUT) of 149.6 ± 10.6 pA (n = 18). Although the hypoOUT reversed at 83.7 ± 3.8 mV (n = 18), the posthypoOUT did not reverse. The K+ATP-blocking sulphonylureas tolbutamide (100 µM) and glibenclamide (30 µM), significantly reduced the peak of the hypoOUT by 47.6 ± 7.7% (n = 16) and 54.18 ± 7.5% (n = 3), respectively. In contrast, they did not affect the posthypoOUT. Extracellular barium (300 µM to 1 mM) almost abolished the hypoOUT, leaving the posthypoOUT unchanged. The large K+ channel blocker charybdotoxin (10-50 nM), depressed the hypoOUT after tolbutamide treatment. To investigate whether or not cytosolic factors might control the development of the hypoOUT, we dialyzed the principal neurons by patch-clamp recordings (Vh 60 mV). Under whole cell recordings hypoxia evoked an hypoOUT of 70.2 ± 14.5 pA that reversed polarity at 87.9 ± 5.1 mV (n = 8). A small posthypoxic response was detected upon reoxygenation in a few neurons (4 out of 14). Three different sulphonylureas, tolbutamide (100 µM), glibenclamide (10-30 µM), and glipizide (100 nM) completely blocked the hypoOUT in patch-clamped neurons. The hypoOUT was also abolished by extracellular BaCl2 (300 µM). When the content of ATP in the dialyzate was raised from 2 to 10 mM no outward current/hyperpolarization was evoked by hypoxia. These data suggest that the hypoOUT, in principal neurons, is a complex response sustained by at least two barium-sensitive components: 1) an ATP-dependent, sulphonylurea-sensitive K+ conductance which could be isolated by the patch-clamp techniques and 2) a K+ conductance remaining after tolbutamide in intracellularly recorded neurons, which is sensitive to charybdotoxin and dependent on dialyzable cytosolic factors.
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