Intestinal fat differentially suppresses sham feeding of liquid diets and preferred gustatory stimuli. Although the behavioral effect is robust, no electrophysiological evidence exists to account for its neural basis. Therefore, we investigated the effect of intestinal fat on gustatory coding in the pontine parabrachial nuclei (PBN) by recording from single neurons in awake rats before, during, and after intraduodenal infusions of lipid (Intralipid; 10 ml, 5 kcal). Intraduodenal lipid did not alter the response profiles of PBN taste neurons. It did, however, produce an overall decrease in response magnitude (-16.25%; n = 43), with the largest reduction to sucrose (-30%; n = 43). The most pronounced suppression occurred in sucrose- best neurons in response to sucrose (-55%; n = 19), and this effect was largest for the sucrose-specific cells (-77%; n = 3). After lipid infusions, nonspecific neurons in both the sucrose-best and NaCl-best categories also responded less to their best stimulus (sucrose, -46%; n = 16; NaCl, -35%; n = 13). In contrast, no significant changes were found in NaCl-specific cells in response to NaCl. All effects appeared with short latency (~5 min) and were reversible within the time frame of a meal. In controls, duodenal infusions of saline did not cause any changes in taste responsiveness. These results suggest that intestinal fat has specific effects on taste coding in the PBN that may contribute to the intake suppression of palatable food observed in behavioral studies. The similar, short latency of both the behavioral and neural effects supports the hypothesis of a preabsorptive site of action.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Neuroscience|
|State||Published - Aug 15 1999|
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