title: A comparison of voluntary salt-intake behavior in Nax-gene deficient and wild-type mice with reference to peripheral taste inputs.
abstract: The Na(x) channel, a subfamily of voltage-gated sodium channels, is thought to be a specific sodium receptor in the central nervous system. Our previous study revealed that Na(x)-gene-deficient mice consumed excessive amounts of NaCl even under water-deprived conditions. In the present study, to investigate whether the peripheral taste inputs are involved in the abnormal intake of salt in Na(x)-deficient mice (homo), voluntary intake of various taste solutions in homo and wild-type mice (wild) was examined under non-deprived conditions. Homo showed a higher preference for 0.15 M NaCl solution than wild. Preference ratios for other basic tastants were identical between groups. Transection of the chorda tympani (CT) or the glossopharyngeal (GP) nerve had little effect on salt-intake behavior in homo and wild. Although combined transection of the superior laryngeal (SL) and GP nerves decreased NaCl intake in homo but not in wild, there were no differences in preference ratios for NaCl in homo before and after SL+GP transection. On the other hand, preference ratios for NaCl in wild tended to increase after combined SL and GP transection. Consequently, preference ratios for NaCl after SL+GP transection were no different between homo and wild. While electrophysiological responses of the CT and the GP to various taste solutions were indistinguishable between homo and wild, those of the SL to NaCl in homo were smaller than those in wild only at lower concentrations (0.01 and 0.03 M). Thus, chemosensory inputs from the oro-pharyngeal regions had little effect on abnormal salt intake in homo, if any. From these results, it is suggested that the higher preference for NaCl in homo is mainly due to the lack of Na(x) channels in the central nervous system.
authors.affiliation: Department of Behavioral Physiology, Graduate School of Human Sciences, Osaka University, 1-2 Yamadaoka, Suita, Japan.
authors.forename: Uno
authors.initials: U
authors.lastname: Watanabe
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Shimura
authors.forename: Noritaka
authors.initials: N
authors.lastname: Sako
authors.forename: Jun-ichi
authors.initials: J
authors.lastname: Kitagawa
authors.forename: Tomio
authors.initials: T
authors.lastname: Shingai
authors.forename: Eiji
authors.initials: E
authors.lastname: Watanabe
authors.forename: Masaharu
authors.initials: M
authors.lastname: Noda
authors.forename: Takashi
authors.initials: T
authors.lastname: Yamamoto
mesh_terms: D000818:Animals; D002755:Choice Behavior / Q000502:physiology*; D004327:Drinking Behavior / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010525:Peripheral Nerves / Q000502:physiology; D015222:Sodium Channels / Q000172:deficiency* / Q000235:genetics; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D013649:Taste / Q000235:genetics* / Q000502:physiology; D061566:Voltage-Gated Sodium Channels
chemical_list: C503483:Scn7a protein, mouse; D015222:Sodium Channels; D017673:Sodium Chloride, Dietary; D061566:Voltage-Gated Sodium Channels