JN Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Neurophysiol 83: 192-197, 2000;
0022-3077/00 $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 ISI Web of Science
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 ISI Web of Science (17)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Seutin, V.
Right arrow Articles by Dresse, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Seutin, V.
Right arrow Articles by Dresse, A.

The Journal of Neurophysiology Vol. 83 No. 1 January 2000, pp. 192-197
Copyright ©2000 by the American Physiological Society

Calcium Release From Internal Stores Is Required for the Generation of Spontaneous Hyperpolarizations in Dopaminergic Neurons of Neonatal Rats

Vincent Seutin, Fatiha Mkahli, Laurent Massotte, and Albert Dresse

Laboratory of Pharmacology, University of Liège, Tour de Pathologie (B23), B-4000 Sart Tilman/Liège 1, Belgium

Seutin, Vincent, Fatiha Mkahli, Laurent Massotte, and Albert Dresse. Calcium Release From Internal Stores Is Required for the Generation of Spontaneous Hyperpolarizations in Dopaminergic Neurons of Neonatal Rats. J. Neurophysiol. 83: 192-197, 2000. We recently have demonstrated the existence of spontaneous hyperpolarizations in midbrain dopaminergic neurons of neonatal but not adult rats. These events are mediated by the opening of apamin-sensitive K+ channels after a rise in the intracellular concentration of Ca2+. They are resistant to tetrodotoxin in most cases and are probably endogenous (i.e., not synaptically activated). Here their mechanism was investigated. Cyclopiazonic acid (10 µM), a specific inhibitor of endoplasmic reticulum Ca2+ ATPases, reversibly abolished the events. Caffeine, which promotes Ca2+ release from intracellular stores, had concentration-dependent effects. At 1 mM, it markedly and steadily increased the frequency and the amplitude of the hyperpolarizations. At 10 mM, it induced a transient increase in their frequency followed by their cessation. All these effects were quickly reversible. Ryanodine (10 µM), which decreases the conductance of Ca2+ release channels, irreversibly blocked the spontaneous hyperpolarizations. Dantrolene (100 µM), a blocker of Ca2+ release from sarcoplasmic reticulum of striated muscle, did not affect the events. On the other hand, Cd2+ (100-300 µM), a broad antagonist of membrane voltage-gated Ca2+ channels, significantly reduced the amplitude and the frequency of the hyperpolarizations. However, when the frequency of the events was increased by 1 mM caffeine, Cd2+ affected them to a smaller extent, whereas cyclopiazonic acid still abolished them. We conclude that internal stores are the major source of Ca2+ ions that induce the K+ channel openings underlying the spontaneous hyperpolarizations of these neurons.




This article has been cited by other articles:


Home page
 J. Neurophysiol.Home page
C. C. Canavier, S. A. Oprisan, J. C. Callaway, H. Ji, and P. D. Shepard
Computational Model Predicts a Role for ERG Current in Repolarizing Plateau Potentials in Dopamine Neurons: Implications for Modulation of Neuronal Activity
J Neurophysiol, November 1, 2007; 98(5): 3006 - 3022.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
Y. Yanovsky, S. Velte, and U. Misgeld
Ca2+ release-dependent hyperpolarizations modulate the firing pattern of juvenile GABA neurons in mouse substantia nigra pars reticulata in vitro
J. Physiol., December 15, 2006; 577(3): 879 - 890.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
A. Verkhratsky
Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons
Physiol Rev, January 1, 2005; 85(1): 201 - 279.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
G. Cui, T. Okamoto, and H. Morikawa
Spontaneous Opening of T-Type Ca2+ Channels Contributes to the Irregular Firing of Dopamine Neurons in Neonatal Rats
J. Neurosci., December 8, 2004; 24(49): 11079 - 11087.
[Abstract] [Full Text] [PDF]

Home page
 J. Cell Sci.Home page
Y. M. Choi, S. H. Kim, D. Y. Uhm, and M. K. Park
Glutamate-mediated [Ca2+]c dynamics in spontaneously firing dopamine neurons of the rat substantia nigra pars compacta
J. Cell Sci., July 1, 2003; 116(13): 2665 - 2675.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
J. Wolfart and J. Roeper
Selective Coupling of T-Type Calcium Channels to SK Potassium Channels Prevents Intrinsic Bursting in Dopaminergic Midbrain Neurons
J. Neurosci., May 1, 2002; 22(9): 3404 - 3413.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
J. Wolfart, H. Neuhoff, O. Franz, and J. Roeper
Differential Expression of the Small-Conductance, Calcium-Activated Potassium Channel SK3 Is Critical for Pacemaker Control in Dopaminergic Midbrain Neurons
J. Neurosci., May 15, 2001; 21(10): 3443 - 3456.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
H. Morikawa, F. Imani, K. Khodakhah, and J. T. Williams
Inositol 1,4,5-Triphosphate-Evoked Responses in Midbrain Dopamine Neurons
J. Neurosci., October 15, 2000; 20(20): RC103 - RC103.
[Abstract] [Full Text] [PDF]


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