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J Neurophysiol 80: 2237-2243, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 80 No. 5 November 1998, pp. 2237-2243
Copyright ©1998 The American Physiological Society

Intracellular Sodium and Calcium Homeostasis During Hypoxia in Dopamine Neurons of Rat Substantia Nigra Pars Compacta

Ezia Guatteo1, Nicola B. Mercuri1, 2, Giorgio Bernardi1, 2, and Thomas Knöpfel1, 3

1 Department of Pharmacology, Istituto di Ricovero e Cura a Carattere Scientifico, Ospedale S. Lucia, 00179 Rome; 2 Clinica Neurologica, Università di Tor Vergata, 00133 Rome, Italy; and 3 Laboratory for Neuronal Circuit Dynamics, Brain Science Institute, The Institute of Physical and Chemical Research, Saitama 351-0198, Japan

Guatteo, Ezia, Nicola B. Mercuri, Giorgio Bernardi, and Thomas Knöpfel. Intracellular sodium and calcium homeostasis during hypoxia in dopamine neurons of rat substantia nigra pars compacta. J. Neurophysiol. 80: 2237-2243, 1998. We investigated the hypoxia-induced disturbance of cytosolic sodium concentration ([Na+]i) and of cytosolic calcium concentration ([Ca2+]i) in dopamine neurons of the substantia nigra pars compacta in rat midbrain slices, by combining whole cell patch-clamp recordings and microfluorometry. Transient hypoxia (3-5 min) induced an outward current (118.7 ± 15.1 pA, mean ± SE; VH = -60 mV). The development of this outward current was associated with an elevation in [Na+]i and in [Ca2+]i. The hypoxia-induced outward current as well as the elevations in [Na+]i and [Ca2+]i were not affected by the ionotropic and metabotropic glutamate receptor antagonists D-amino-phosphonovalerate (50 µM), 6nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione (10 µM) and S-(alpha )-methyl-4-carboxyphenylglycine (500 µM). Tolbutamide, a blocker of ATP-dependent K+ channels, depressed the hypoxia-induced outward current but did not affect the increases in [Na+]i or [Ca2+]i. Increasing the concentration of ATP in the internal solution from 2 to 10 mM strongly reduced the hypoxia-induced outward current but did not reduce the rise in [Na+]i. Decreasing the concentration of extracellular Na+ to 19.2 mM depressed the hypoxia-induced outward current and resulted in a decrease in resting [Na+]i. Under this condition hypoxia still increased [Na+]i, albeit to levels not exceeding those of resting [Na+]i observed under control conditions. We conclude that 1) a major component of the hypoxia-induced outward current of these cells is caused by a depletion of intracellular ATP in combination with an increase in [Na+]i, 2) that the [Na+]i and [Ca2+]i responses are not mediated by glutamate receptors, 3) that the [Na+]i and [Ca2+]i responses are not depressed by activation of sulfonylurea receptors, and 4) that the rise in [Na+]i induced by short-lasting hypoxia is not due to a ATP depletion-induced failure of Na+ extrusion.




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