Journal
FRONTIERS IN INTEGRATIVE NEUROSCIENCE
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fnint.2019.00035
Keywords
high fat diet; obesity; taste; nucleus of the solitary tract; electrophysiology; gustatory; rat
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Funding
- NIDCD [RO1 DC6013904]
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Taste perception changes with obesity but the underlying neural changes remain poorly understood. To address this issue, we recorded taste responses from single cells in the nucleus tractus solitarius (NTS, the first synapse in the central gustatory circuit) in awake, diet-induced obese [(DIO; >= 8 weeks on a high-energy diet (45% fat, 17% sugar; HED)], and lean rats. Rats were implanted with a bundle of microelectrodes in the NTS and allowed to recover. Water-deprived rats were allowed to freely lick various tastants in an experimental chamber. Taste stimuli included an array of sapid stimuli dissolved in artificial saliva (AS). Each taste trial consisted of five consecutive licks followed by five AS licks presented on a VR5 schedule. Results showed that taste responses (n = 49 for DIO; n = 74 for lean rats) in NTS cells in DIO rats were smaller in magnitude, shorter in duration, and longer in latency that those in lean rats. However, there were proportionately more taste-responsive cells in DIO than in lean rats. Lick coherence in DIO rats was significantly lower than in lean rats, both in taste-responsive, and lick-related cells (n = 172 in lean; n = 65 in DIO). Analyses of temporal coding showed that taste cells in DIO rats conveyed less information about taste quality than cells in lean rats. Collectively, results suggest that a HED produces blunted, but more prevalent, responses to taste in the NTS, and a weakened association of taste responses with ingestive behavior. These neural adaptations may represent both negative effects and compensatory mechanisms of a HED that may underlie deficits in taste-related behavior associated with obesity.
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