title: High salt recruits aversive taste pathways.
abstract: In the tongue, distinct classes of taste receptor cells detect the five basic tastes; sweet, sour, bitter, sodium salt and umami. Among these qualities, bitter and sour stimuli are innately aversive, whereas sweet and umami are appetitive and generally attractive to animals. By contrast, salty taste is unique in that increasing salt concentration fundamentally transforms an innately appetitive stimulus into a powerfully aversive one. This appetitive-aversive balance helps to maintain appropriate salt consumption, and represents an important part of fluid and electrolyte homeostasis. We have shown previously that the appetitive responses to NaCl are mediated by taste receptor cells expressing the epithelial sodium channel, ENaC, but the cellular substrate for salt aversion was unknown. Here we examine the cellular and molecular basis for the rejection of high concentrations of salts. We show that high salt recruits the two primary aversive taste pathways by activating the sour- and bitter-taste-sensing cells. We also demonstrate that genetic silencing of these pathways abolishes behavioural aversion to concentrated salt, without impairing salt attraction. Notably, mice devoid of salt-aversion pathways show unimpeded, continuous attraction even to very high concentrations of NaCl. We propose that the 'co-opting' of sour and bitter neural pathways evolved as a means to ensure that high levels of salt reliably trigger robust behavioural rejection, thus preventing its potentially detrimental effects on health.
authors: Howard Hughes Medical Institute and Department of Biochemistry and Molecular Biophysics, Columbia College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
authors: Yuki
authors: Y
authors: Oka
authors: Matthew
authors: M
authors: Butnaru
authors: Lars
authors: L
authors: von Buchholtz
authors: Nicholas J P
authors: NJ
authors: Ryba
authors: Charles S
authors: CS
authors: Zuker
mesh_terms: D000818:Animals; D001066:Appetite / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D005247:Feeding Behavior / Q000187:drug effects / Q000502:physiology; D020868:Gene Silencing; D051379:Mice; D018345:Mice, Knockout; D009154:Mutation / Q000235:genetics; D054799:Phospholipase C beta / Q000172:deficiency / Q000235:genetics / Q000378:metabolism; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage / Q000494:pharmacology*; D050053:TRPM Cation Channels / Q000172:deficiency / Q000235:genetics / Q000378:metabolism; D013649:Taste / Q000187:drug effects* / Q000235:genetics / Q000502:physiology*; D013650:Taste Buds / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*
chemical_list: D017673:Sodium Chloride, Dietary; D050053:TRPM Cation Channels; C498617:Trpm5 protein, mouse; D054799:Phospholipase C beta; C518037:Plcb2 protein, mouse