Integration of gastric distension and gustatory responses in the parabrachial nucleus

Palatable gustatory stimuli promote feeding, whereas gastric distension gen erally inhibits this behavior. We explored a neural basis for integration o f these opposing sensory signals by evaluating the effect of gastric disten sion on gustatory responses in the parabrachial nucleus (PBN) of anesthetiz ed rats. Sixteen percent of 92 taste cells were coactivated; they responded to independent taste or gastric distension stimulus application. Modulatio n of taste responses by distension was more prevalent; taste responses decl ined 37% in response to distension in 25% of the cells and increased by 46% in 10% of cells. Across the whole population, however, the suppressive eff ect of distension on taste responses was small (6%). The incidence of modul ation did not vary as a simple hedonic function of gustatory sensitivity, i .e., similar proportions of sucrose-, citric- acid-, and QHCl- best, but no t NaCl-best, neurons were modulated by gastric distension. Coactivated, mod ulated, and nonmodulated gustatory-responsive cells were intermingled in th e gustatory zone of the caudal PBN. The suppression of PBN taste responses by visceral stimulation may reflect a mechanism for satiation and further i mplicates the PBN in the control of ingestive function.