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This Article Full Text Full Text (PDF) Supplemental data All Versions of this Article: 578/2/481    most recent jphysiol.2006.119008v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gover, T. D. Articles by Weinreich, D. Search for Related Content PubMed PubMed Citation Articles by Gover, T. D. Articles by Weinreich, D. Related Collections Neuroscience

¹ The Neuroscience Program, University of Maryland, Baltimore, MD 21201-1559, USA
² Medical Biotechnology Center, University of Maryland Biotechnology Institute, and Departments of
³ Physiology
⁴ Pharmacology and Experimental Therapeutics, University of Maryland, School of Medicine, Baltimore, MD 21201-1559, USA
⁵ Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo, Brazil 31270-901

Ca²⁺ is vital for release of neurotransmitters and trophic factors from peripheral sensory nerve terminals (PSNTs), yet Ca²⁺ regulation in PSNTs remains unexplored. To elucidate the Ca²⁺ regulatory mechanisms in PSNTs, we determined the effects of a panel of pharmacological agents on electrically evoked Ca²⁺ transients in rat corneal nerve terminals (CNTs) in vitro that had been loaded with the fluorescent Ca²⁺ indicator, Oregon Green 488 BAPTA-1 dextran or fura-2 dextran in vivo. Inhibition of the sarco(endo)plasmic reticulum Ca²⁺-ATPase, disruption of mitochondrial Ca²⁺ uptake, or inhibition of the Na⁺–Ca²⁺ exchanger did not measurably alter the amplitude or decay kinetics of the electrically evoked Ca²⁺ transients in CNTs. By contrast, inhibition of the plasma membrane Ca²⁺-ATPase (PMCA) by increasing the pH slowed the decay of the Ca²⁺ transient by 2-fold. Surprisingly, the energy for ion transport across the plasma membrane of CNTs is predominantly from glycolysis rather than mitochondrial respiration, as evidenced by the observation that Ca²⁺ transients were suppressed by iodoacetate but unaffected by mitochondrial inhibitors. These observations indicate that, following electrical activity, the PMCA is the predominant mechanism of Ca²⁺ clearance from the cytosol of CNTs and glycolysis is the predominant source of energy.

(Received 10 August 2006; accepted after revision 6 November 2006; first published online 9 November 2006)
Corresponding author D. Weinreich: Department of Pharmacology and Experimental Therapeutics, University of Maryland, School of Medicine, Bressler Research Building, Room 4-002, 655 West Baltimore Street, Baltimore, MD 21201-1559, USA. Email: dweinrei{at}umaryland.edu

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