JN AJP: Lung Cellular and Molecular Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Neurophysiol 80: 2237-2243, 1998;
0022-3077/98 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Guatteo, E.
Right arrow Articles by Knöpfel, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Guatteo, E.
Right arrow Articles by Knöpfel, T.

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.




This article has been cited by other articles:


Home page
 Cereb CortexHome page
D. Chao, A. Bazzy-Asaad, G. Balboni, S. Salvadori, and Y. Xia
Activation of DOR Attenuates Anoxic K+ Derangement via Inhibition of Na+ Entry in Mouse Cortex
Cereb Cortex, September 1, 2008; 18(9): 2217 - 2227.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
M. Giustizieri, M. L. Cucchiaroni, E. Guatteo, G. Bernardi, N. B. Mercuri, and N. Berretta
Memantine Inhibits ATP-Dependent K+ Conductances in Dopamine Neurons of the Rat Substantia Nigra Pars Compacta
J. Pharmacol. Exp. Ther., August 1, 2007; 322(2): 721 - 729.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
E. Guatteo, C. P. Bengtson, G. Bernardi, and N. B. Mercuri
Voltage-Gated Calcium Channels Mediate Intracellular Calcium Increase in Weaver Dopaminergic Neurons During Stimulation of D2 and GABAB Receptors
J Neurophysiol, December 1, 2004; 92(6): 3368 - 3374.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
H. Neuhoff, A. Neu, B. Liss, and J. Roeper
Ih Channels Contribute to the Different Functional Properties of Identified Dopaminergic Subpopulations in the Midbrain
J. Neurosci., February 15, 2002; 22(4): 1290 - 1302.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
S. Marinelli, M. Federici, P. Giacomini, G. Bernardi, and N. B. Mercuri
Hypoglycemia Enhances Ionotropic But Reduces Metabotropic Glutamate Responses in Substantia Nigra Dopaminergic Neurons
J Neurophysiol, March 1, 2001; 85(3): 1159 - 1166.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
A. Kulik, S. Trapp, and K. Ballanyi
Ischemia But Not Anoxia Evokes Vesicular and Ca2+-Independent Glutamate Release In the Dorsal Vagal Complex In Vitro
J Neurophysiol, May 1, 2000; 83(5): 2905 - 2915.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
E. Guatteo, N. B. Mercuri, G. Bernardi, and T. Knopfel
Group I Metabotropic Glutamate Receptors Mediate an Inward Current in Rat Substantia Nigra Dopamine Neurons That Is Independent From Calcium Mobilization
J Neurophysiol, October 1, 1999; 82(4): 1974 - 1981.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online