Gustatory stimuli representing different perceptual qualities elicit distinct patterns of neuropeptide secretion from taste buds.
Gustatory stimuli representing different perceptual qualities elicit distinct patterns of neuropeptide secretion from taste buds.
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DOI：
10.1523/jneurosci.0372-13.2013
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发表时间：
2013-04-24
期刊：
影响因子：
--
通讯作者：
Munger SD
中科院分区：
文献类型：
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作者：
Geraedts MC;Munger SD
唤起不同感知品质的味觉刺激（例如，甜、鲜、苦、酸、咸）通过味蕾细胞的专用亚群检测，所述味蕾细胞采用感觉受体和转导分子的不同组合。在这里，我们报告说，味觉刺激也引起了独特的模式，神经肽分泌与这些感知品质的味蕾。我们测量了Tas 1 r3 +/+、+/−和−/−小鼠轮廓乳头的胰高血糖素样肽-1（GLP-1）、胰高血糖素和神经肽Y（NPY）的味素依赖性分泌。将分离的舌上皮细胞安装在改良的Ussing室中，允许味蕾的顶端刺激;从基底侧收集分泌的肽，并通过特异性ELISA进行测量。食欲刺激（甜：葡萄糖、三氯蔗糖;鲜味：谷氨酸盐;多糖：多糖）引起GLP-1和NPY分泌，并抑制基础胰高血糖素分泌。甜味和鲜味刺激在Tas 1 r3 −/−小鼠中无效，表明甜味和鲜味味觉受体共同的T1 R3亚基的强制性作用。多糖反应不受T1 R3缺失的影响，与不同多糖味觉受体的存在一致。甜味刺激对肽分泌的影响也需要关闭ATP敏感性K+（KATP）通道，因为KATP通道激活剂二氮嗪抑制葡萄糖和三氯蔗糖对GLP-1和胰高血糖素释放的影响。酸柠檬酸和盐NaCl都增加了NPY的分泌，但对GLP-1或胰高血糖素没有影响。苦地那铵对这些肽没有影响。总之，这些结果表明，不同的感知品质的味觉刺激引起味蕾的神经肽分泌的独特模式。
Taste stimuli that evoke different perceptual qualities (e.g., sweet, umami, bitter, sour, salty) are detected by dedicated subpopulations of taste bud cells that employ distinct combinations of sensory receptors and transduction molecules. Here, we report that taste stimuli also elicit unique patterns of neuropeptide secretion from taste buds that are correlated with those perceptual qualities. We measured tastant-dependent secretion of glucagon-like peptide-1 (GLP-1), glucagon and neuropeptide Y (NPY) from circumvallate papillae of Tas1r3+/+, +/− and −/− mice. Isolated tongue epithelia were mounted in modified Ussing chambers, permitting apical stimulation of taste buds; secreted peptides were collected from the basal side and measured by specific ELISAs. Appetitive stimuli (sweet: glucose, sucralose; umami: monosodium glutamate; polysaccharide: Polycose) elicited GLP-1 and NPY secretion and inhibited basal glucagon secretion. Sweet and umami stimuli were ineffective in Tas1r3−/− mice, indicating an obligatory role for the T1R3 subunit common to the sweet and umami taste receptors. Polycose responses were unaffected by T1R3 deletion, consistent with the presence of a distinct polysaccharide taste receptor. The effects of sweet stimuli on peptide secretion also required the closing of ATP-sensitive K+ (KATP) channels, as the KATP channel activator diazoxide inhibited the effects of glucose and sucralose on both GLP-1 and glucagon release. Both sour citric acid and salty NaCl increased NPY secretion but had no effects on GLP-1 or glucagon. Bitter denatonium showed no effects on these peptides. Together, these results suggest that taste stimuli of different perceptual qualities elicit unique patterns of neuropeptide secretion from taste buds.