Abstract
The present study reports two experiments that evaluated the influence of bilateral ibotenic acid lesions of the viscerosensory neurons in the lateral parabrachial nucleus (LPBN) on intake of four prototypical taste stimuli (sucrose, sodium chloride, citric acid, and quinine hydrochloride). In the 24-h, two-bottle tests of Experiment 1, rats with lesions of the LPBN were severely impaired in their concentration-dependent consumption of sucrose, displayed a mild disturbance of sodium chloride intake, and drank normal amounts of citric acid and quinine hydrochloride. These lesion-induced deficits were less pronounced when assessed with the 15-min, 1-bottle tests of Experiment 2. The results suggest that destruction of the viscerosensory neurons within the LPBN disrupt the processing of gastrointestinal feedback.
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