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Acute sodium deficiency reduces gustatory responsiveness to NaCl in the parabrachial nucleus of rats.

作者信息

Shimura T, Komori M, Yamamoto T

机构信息

Department of Behavioral Physiology, Faculty of Human Sciences, Osaka University, Suita, Japan.

出版信息

Neurosci Lett. 1997 Oct 24;236(1):33-6. doi: 10.1016/s0304-3940(97)00745-3.

Abstract

Sodium-deprived rats ingest excessive amounts of salt solutions at high concentrations which are normally avoided. This phenomenon, salt appetite, is known to be controlled by the sense of taste. In the present study, a possible involvement of the parabrachial nucleus (PBN) in sodium appetite was examined by recording PBN neuron responses to 12 different taste stimuli in sodium-deprived and control groups of urethane anesthetized rats. Sodium deficiency was induced by two injections of furosemide 24 and 22 h before the recording. Taste responses to 0.3 and 0.5 M solutions of NaCl were significantly lower in the sodium-deprived rats than in controls. In gustatory responses to other taste solutions except for quinine hydrochloride solution, no differences were detected between the two groups of the rats. Correlation coefficients of responses among sodium salts and those between 0.5 M NaCl and sweeteners were larger in the sodium-deprived rats than in controls. The results indicate that PBN neurons in sodium-deprived rats are critically implicated in induction of quantitative and qualitative changes of gustatory sense to sodium salts.

摘要

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