Mechanisms of itch evoked by β-alanine.

Mechanisms of itch evoked by β-alanine.
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DOI:
10.1523/jneurosci.3509-12.2012
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发表时间:
2012-10-17
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
通讯作者:
Dong X
Dong X
中科院分区:
其他
文献类型:
--
作者:
Liu Q;Sikand P;Ma C;Tang Z;Han L;Li Z;Sun S;LaMotte RH;Dong X

文献摘要

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β-丙氨酸是一种流行的增肌补充剂,食用后会引起瘙痒和刺痛,但其潜在的分子和神经机制尚不清楚。本研究表明,在小鼠中,β-丙氨酸引发瘙痒相关行为,这需要MrgprD,一种由初级感觉神经元亚群表达的G蛋白偶联受体。这些神经元专门支配皮肤,对β-丙氨酸、热和机械有害刺激有反应,但对组胺没有反应。在人类中,皮内注射β-丙氨酸引起瘙痒,但既没有轮状也没有耀斑,这表明瘙痒不是由组胺介导的。因此,对β-丙氨酸有反应的初级感觉神经元可能是组胺独立的瘙痒神经回路的一部分,也是治疗抗组胺药无法缓解的临床瘙痒的靶点。
β-alanine, a popular supplement for muscle building, induces itch and tingling after consumption, but the underlying molecular and neural mechanisms are obscure. Here we show that, in mice, β-alanine elicited itch-associated behavior that requires MrgprD, a G protein-coupled receptor expressed by a subpopulation of primary sensory neurons. These neurons exclusively innervate the skin, respond to β-alanine, heat and mechanical noxious stimuli but do not respond to histamine. In humans, intradermally injected β-alanine induced itch but neither wheal nor flare suggesting that the itch was not mediated by histamine. Thus, the primary sensory neurons responsive to β-alanine are likely part of a histamine-independent itch neural circuit and a target for treating clinical itch that is unrelieved by anti-histamines.