Calcium‐activated chloride current in normal mouse sympathetic ganglion cells.

Abstract

1. In rat sympathetic ganglion cells, axotomy induces the appearance of a depolarizing afterpotential (ADP) produced by a calcium-activated chloride current. Here we report that this current is also present in normal sympathetic neurones from the mouse. 2. In an in vitro preparation of the superior cervical ganglion, an ADP was observed after spike firing in 50% of the cells studied with single-electrode current-and voltage-clamp techniques. 3. When the cells were voltage clamped at -50 mV in the presence of tetrodotoxin (ITX) and tetraethylammonium chloride (TEA), depolarizing jumps evoked inward calcium currents which were contaminated by outward chloride currents, followed by slowly decaying inward chloride tail currents. 4. The ADP and the inward tail currents disappeared when calcium was removed from the extracellular solution or when cadmium was added. 5. The reversal potential for the inward tail current was approximately -24 mV and was displaced in agreement with the Nernst equation for chloride when the extracellular NaCl was replaced by sucrose or sodium isethionate. The chloride channel blocker anthracene-9-carboxylic acid (9AC) inhibited both the ADP and the tail current. 6. Using intracellular injection of neurobiotin, we found that cells with shorter dendrites had larger ADPs. In axotomized ganglia practically all cells showed very pronounced ADPs. 7. We conclude that normal mouse sympathetic ganglion cells have a calcium-activated chloride current that generates an ADP. The channels responsible for this current are probably located in the dendrites.

Modulation of Silent and Constitutively Active Nociceptin/Orphanin FQ Receptors by Potent Receptor Antagonists and Na+ Ions in Rat Sympathetic Neurons

“…NMG was the major monovalent cation in the external solution in which Na ϩ was absent and was substituted for an equimolar amount of Na ϩ in the 120 mM Na ϩ external solution. NaMeSO 3 rather than NaCl was used in the external solutions to maintain equal Cl Ϫ ion concentrations in both internal and external solutions (20 mM) with a predicted reversal potential of Cl Ϫ currents at 0 mV (Zhu and Ikeda, 1993) and to avoid contamination of Ca 2ϩ -activated Cl Ϫ currents expressed in sympathetic neurons (De Castro et al, 1997). Nevertheless, in some experiments, NaCl was used, and similar results were observed (data not shown).…”

Interaction between calcium-activated chloride channels and the cystic fibrosis transmembrane conductance regulator

“…They are characterized by strong outward rectification, delayed activation at positive potentials but fast inactivation at negative potentials [3,17,24]. In excitable cells, they control excitation via generation of afterpotentials, shaping the action potential and the modulation of oscillatory changes in in-tracellular calcium concentration, [Ca 2+ ] i [4,5,19]. They are of paramount importance in non-excitable, secretory cells, including epithelial cells from different gland tissues and intestine [8,11].…”

Axotomy-Induced Expression of Calcium-Activated Chloride Current in Subpopulations of Mouse Dorsal Root Ganglion Neurons

“…This result is particularly relevant given that specific ionic modifications induced by nerve injury have been demonstrated exclusively within the small nociceptive population . In naive sensory and axotomized sympathetic neurons, I Cl(Ca) was shown to promote afterdepolarization after spike firing (De Castro et al 1997;Mayer 1985), and its increased expression in axotomized DRG neurons could thus contribute to their enhanced excitability. In future studies, determination of the chloride homeostasis as well as of the physiological activator of I Cl(Ca) should provide clues to understand I Cl(Ca) contribution to electrical activity.…”

“…They persist under physiological conditions, in a subset of postnatal and adult dorsal root ganglion (DRG) neurons (Abdulla and Smith 1999;Currie and Scott 1992;Lovinger and White 1989). In naive DRG neurons, I Cl(Ca) activation promotes afterdepolarization after spike firing (De Castro et al 1997;Mayer 1985), and in adult sympathetic and nodose ganglion neurons, I Cl(Ca) expression is upregulated by axotomy (Lancaster et al 2002;Sanchez-Vives and Gallego 1994). Besides a potential role in electrical activity, I Cl(Ca) has been shown to be involved in other cellular functions such as apoptosis, cell adhesion, and possibly volume regulation.…”