Dept. of Psychological Sciences, 703 Third St., Purdue Univ., West Lafayette, IN 47907, USA.
Am J Physiol Regul Integr Comp Physiol. 2011 Nov;301(5):R1557-68. doi: 10.1152/ajpregu.00344.2011. Epub 2011 Aug 24.
The discovery that cells in the gastrointestinal (GI) tract express the same molecular receptors and intracellular signaling components known to be involved in taste has generated great interest in potential functions of such post-oral "taste" receptors in the control of food intake. To determine whether taste cues in the GI tract are detected and can directly influence behavior, the present study used a microbehavioral analysis of intake, in which rats drank from lickometers that were programmed to simultaneously deliver a brief yoked infusion of a taste stimulus to the intestines. Specifically, in daily 30-min sessions, thirsty rats with indwelling intraduodenal catheters were trained to drink hypotonic (0.12 M) sodium chloride (NaCl) and simultaneously self-infuse a 0.12 M NaCl solution. Once trained, in a subsequent series of intestinal taste probe trials, rats reduced licking during a 6-min infusion period, when a bitter stimulus denatonium benzoate (DB; 10 mM) was added to the NaCl vehicle for infusion, apparently conditioning a mild taste aversion. Presentation of the DB in isomolar lithium chloride (LiCl) for intestinal infusions accelerated the development of the response across trials and strengthened the temporal resolution of the early licking suppression in response to the arrival of the DB in the intestine. In an experiment to evaluate whether CCK is involved as a paracrine signal in transducing the intestinal taste of DB, the CCK-1R antagonist devazepide partially blocked the response to intestinal DB. In contrast to their ability to detect and avoid the bitter taste in the intestine, rats did not modify their licking to saccharin intraduodenal probe infusions. The intestinal taste aversion paradigm developed here provides a sensitive and effective protocol for evaluating which tastants-and concentrations of tastants-in the lumen of the gut can control ingestion.
研究发现，胃肠道（GI）细胞表达相同的分子受体和细胞内信号成分，这些受体和信号成分已知参与味觉，这激发了人们对这些口腔后“味觉”受体在控制食物摄入方面的潜在功能的极大兴趣。为了确定胃肠道中的味觉线索是否被检测到并能直接影响行为，本研究使用了一种摄食微行为分析，其中大鼠从舔食计中摄取液体，舔食计被编程为同时向肠道输送短暂的味觉刺激伴随输注。具体来说，在每日 30 分钟的实验中，有留置十二指肠导管的口渴大鼠被训练饮用低渗（0.12M）氯化钠（NaCl）溶液，并同时自行输注 0.12M NaCl 溶液。一旦训练完成，在随后的一系列肠道味觉探针实验中，当将苦味刺激物苯甲地那铵（DB；10mM）添加到 NaCl 载体中进行输注时，大鼠在 6 分钟的输注期间减少舔食，显然是对轻度味觉厌恶进行了条件反射。在肠道输注中使用等渗氯化锂（LiCl）呈现 DB 加速了该反应在各次试验中的发展，并增强了对 DB 进入肠道时早期舔食抑制的时间分辨率。在一项评估 CCK 是否作为旁分泌信号参与转导 DB 的肠道味觉的实验中，CCK-1R 拮抗剂地伐肽部分阻断了对肠道 DB 的反应。与它们在肠道中检测和避免苦味的能力相比，大鼠不会改变对十二指肠内蔗糖探针输注的舔食行为。这里开发的肠道味觉厌恶范式提供了一种敏感有效的方案，用于评估肠道腔中的哪些味觉物质和味觉物质浓度可以控制摄食。
