title: Calcium homeostasis in trigeminal ganglion cell bodies.
abstract: In primary sensory afferent neurons, Ca2+ plays a vital role in the regulation of cellular processes including receptor and synaptic plasticity, neurotransmitter and trophic factor release and gene regulation. Current understanding of the mechanisms underlying Ca2+ homeostasis of primary sensory afferent neurons is mostly derived from studies on dorsal root ganglia and nodose ganglia neuron cell bodies. Little is known about Ca2+ homeostasis in trigeminal ganglion neurons (TGNs). To determine what cellular processes contribute to electrically-evoked Ca2+ transients in TGNs, we probed Ca2+ regulatory mechanisms in TGN cell bodies from the ophthalmic division with a panel of pharmacological reagents. Ca2+ transients were evoked in fura-2 loaded TGNs by depolarizing the plasma membrane with brief (500 ms) puffs of 50 mM KCl. Cyclopiazonic acid (CPA; 5 microM), an inhibitor of the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA), significantly decreased the peak amplitude, and slowed the decay, of the KCl-evoked Ca2+ transients in TGNs. The mitochondrial protonophore, carbonyl cyanide 3-chloro-phenylhydrazone (CCCP; 5 microM) significantly increased the peak amplitude of KCl-evoked Ca2+ transients. These data demonstrate that Ca2+ stores do play a major role in Ca2+ homeostasis in TGN cell bodies. To determine the role of the sodium-calcium exchanger (NCX) in KCl-evoked Ca2+ transients in TGNs, we inhibited the exchanger with KB-R7943 (10 microM), or by replacing Na+ with Li+. NCX inhibition did not affect either the peak amplitude or the decay kinetics of the KCl-evoked Ca2+ transients. Therefore, the NCX does not play a significant role in removing cytosolic Ca2+ from TGNs. To test whether the plasma membrane calcium-ATPase (PMCA) contributes to Ca2+ extrusion, we inhibited its activity by a shift to alkaline pH (9.0). At pH 9.0, both the peak amplitude and decay time of the KCl-evoked Ca2+ transient were increased significantly. These data suggest that, in TGNs, the PMCA is the major mechanism for removing cytosolic Ca2+ following electrical activity.
authors.affiliation: The Neuroscience Program, University of Maryland, School of Medicine, Baltimore, MD 21201-1559, United States.
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 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000502:physiology; D006706:Homeostasis; D008297:Male; D008928:Mitochondria / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D018408:Patch-Clamp Techniques; D053499:Plasma Membrane Calcium-Transporting ATPases / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D019831:Sodium-Calcium Exchanger / Q000502:physiology; D012668:Trigeminal Ganglion / Q000166:cytology / Q000502:physiology*
chemical_list: D015220:Calcium Channels; D019831:Sodium-Calcium Exchanger; D053499:Plasma Membrane Calcium-Transporting ATPases; D002118:Calcium