title: Calcium regulation in individual peripheral sensory nerve terminals of the rat.
abstract: 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.
authors.affiliation: The Neuroscience Program, University of Maryland, Baltimore, MD 21201-1559, USA.
authors.forename: Tony D
authors.initials: TD
authors.lastname: Gover
authors.forename: Thaís H V
authors.initials: TH
authors.lastname: Moreira
authors.forename: Joseph P Y
authors.initials: JP
authors.lastname: Kao
authors.forename: Daniel
authors.initials: D
authors.lastname: Weinreich
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone / Q000031:analogs & derivatives / Q000494:pharmacology; D003315:Cornea / Q000294:innervation; D004558:Electric Stimulation; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006019:Glycolysis / Q000187:drug effects / Q000502:physiology; D006863:Hydrogen-Ion Concentration; D007211:Indoles / Q000494:pharmacology; D007461:Iodoacetates / Q000494:pharmacology; D007476:Ionophores / Q000494:pharmacology; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D010042:Ouabain / Q000494:pharmacology; D053499:Plasma Membrane Calcium-Transporting ATPases / Q000037:antagonists & inhibitors / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D011984:Sensory Receptor Cells / Q000187:drug effects / Q000502:physiology*; D019831:Sodium-Calcium Exchanger / Q000037:antagonists & inhibitors; D013696:Temperature; D013890:Thiourea / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: C101670:2-(2-(4-(4-nitrobenzyloxy)phenyl)ethyl)isothiourea methanesulfonate; D004791:Enzyme Inhibitors; D007211:Indoles; D007461:Iodoacetates; D007476:Ionophores; D019831:Sodium-Calcium Exchanger; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone; D010042:Ouabain; D053499:Plasma Membrane Calcium-Transporting ATPases; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D013890:Thiourea; D002118:Calcium; C000543:cyclopiazonic acid