The Journal of Neurophysiology Vol. 79 No. 2 February 1998, pp. 911-921
Copyright ©1998 The American Physiological Society

Self-Inhibition in Ca²⁺-Evoked Taste Responses: A Novel Tool for Functional Dissection of Salt Taste Transduction Mechanisms

Mamoun A. Kloub, Gerard L. Heck, and John A. Desimone

Department of Physiology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0551

Kloub, Mamoun A., Gerard L. Heck, and John A. DeSimone. Self-inhibition in Ca²⁺-evoked taste receptors: a novel tool for functional dissection of salt taste transduction mechanisms. J. Neurophysiol. 79: 911-921, 1998. Rat chorda tympani (CT) responses to CaCl₂ were obtained during simultaneous current and voltage clamping of the lingual receptive field. Unlike most other salts, CaCl₂ induced negatively directed transepithelial potentials and gave CT responses that were auto-inhibitory beyond a critical concentration. CT responses increased in a dose-dependent manner to ~0.3 M, whereafter they decreased with increasing concentration. At concentrations where Ca²⁺ was self-inhibitory, it also inhibited responses to NaCl, KCl, and NH₄Cl present in mixtures with CaCl₂. Ca²⁺ completely blocked the amiloride-insensitive component of the NaCl CT response, the entire KCl-evoked CT response, and the high-concentration-domain CT responses of NH₄Cl (0.3 M). The overlapping Ca²⁺-sensitivity between the responses of the three Cl salts (Na⁺, K⁺, and NH⁺₄) suggests a common, Ca²⁺-sensitive, transduction pathway. Extracellular Ca²⁺ has been shown to modulate the paracellular pathways in different epithelial cell lines by decreasing the water permeability and cation conductance of tight junctions. Ca²⁺-induced modulation of tight junctions is associated with Ca²⁺ binding to fixed negative sites. This results in a conversion of ion selectivity from cationic to anionic, which we also observed in our system through simultaneous monitoring of the transepithelial potential during CT recording. The data indicate the paracellular pathway as the stimulatory and modulatory site of CaCl₂ taste responses. In addition, they indicate that important transduction sites for NaCl, KCl, and NH₄Cl taste reception are accessible only through the paracellular pathways. More generally, they show that modulation of paracellular transport by Ca²⁺ in an intact epithelium has functional consequences at a systemic level.

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