Adrenalectomy reduces peripheral neural responses to gustatory stimuli in the rat.
In the rat, sodium need leads to an increase in sodium intake, which depends on salt taste sensitivity. The adrenalectomized rat, because of excessive body sodium loss, has been an important animal model for studying the physiological mechanisms underlying salt ingestion. In order to investigate the mediation by peripheral taste responsivity of changes in salt intake, multiunit responses of the chorda tympani nerve to various concentrations of sodium chloride, potassium chloride, lithium chloride, hydrochloric acid, and quinine hydrochloride were recorded from adrenalectomized and control rats. In order to control for a generalized decrease in sensory sensitivity, recordings from the auriculotemporal nerve to tactile stimulation of the pinna were also performed. There were no group differences in amplitude of the integrated neural responses to tactile stimulation. The largest decrease in gustatory responsivity occurred for suprathreshold concentrations of sodium chloride and lithium chloride. The data are discussed with reference to possible mechanisms underlying this neural alteration and to the role that reductions in salt taste responsivity play in mediating increases in salt intake.
D000311:Adrenal Glands / Q000502:physiology*; D000315:Adrenalectomy; D000818:Animals; D002814:Chorda Tympani Nerve / Q000502:physiology; D007473:Ion Channels / Q000502:physiology; D008297:Male; D008340:Mandibular Nerve / Q000502:physiology; D051381:Rats; D012965:Sodium Chloride; D013649:Taste / Q000502:physiology*; D013650:Taste Buds / Q000502:physiology; D013652:Taste Threshold / Q000502:physiology; D014110:Touch / Q000502:physiology
D007473:Ion Channels; D012965:Sodium Chloride