Self-Inhibition in Ca+2-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.
APStracts 4:304N, 1997.
ABSTRACT
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 approximately 0.3 M, whereafter, they decreased with increasing concentration. At concentrations where Ca+2 was self-inhibitory, it also inhibited responses to NaCl, KCl, and NH4Cl present in mixtures with CaCl2. Ca+2 completely blocked 1) the amiloride-insensitive component of the NaCl CT response 2) the entire KCl- evoked CT response and 3) the high-concentration-domain CT responses of NH4Cl (ò 0.3 M). The overlapping Ca+2-sensitivity between the responses of the three Cl- salts (Na+, K+, NH4+) suggests a common, Ca+2-sensitive, transduction pathway. Extracellular Ca+2 has been shown to modulate the paracellular pathways in different epithelial cell lines by decreasing the water permeability and cation conductance of tight junctions. Ca+2-induced modulation of tight junctions is associated with Ca+2 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 Ca+2 in an intact epithelium, has functional consequences at a systemic level. 

Received 24 April 1997; accepted in final form 30 October 1997.
APS Manuscript Number J328-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 14 November 1997