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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Activation of purinergic receptor subtypes modulates odor sensitivity.
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Activation of purinergic receptor subtypes modulates odor sensitivity.

机译：嘌呤能受体亚型的激活调节气味敏感性。

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摘要

Purinergic nucleotides, including ATP and adenosine, are important neuromodulators of peripheral auditory and visual sensory systems (Thorne and Housley, 1996). ATP released by the olfactory epithelium (OE) after noxious stimuli provides a physiological source for a neuromodulatory substance independent of efferent innervation. Here we show that multiple subtypes of purinergic receptors are differentially expressed in olfactory receptor neurons and sustentacular support cells. Activation of purinergic receptors evoked inward currents and increases in intracellular calcium in cultured mouse olfactory receptor neurons. A mouse olfactory epithelial slice preparation and confocal imaging were used to measure changes in intracellular calcium in response to odors, purinergic receptor (P2R) agonists, or combined odor + P2R agonists. Pharmacological studies show that both P2Y and P2X receptor activation by exogenous and endogenous ATP significantly reduces odor responsiveness. Moreover, purinergic receptor antagonists increase the odor-evoked calcium transient, providing direct evidence that endogenous ATP modulates odor sensitivity via activation of multiple purinergic receptor subtypes in olfactory receptor neurons. Odor activation of G-protein-coupled receptors results in increased cAMP production, opening of cyclic nucleotide-gated channels, influx of Ca2+ and Na+, depolarization of the membrane, and activation of voltage- and Ca2+-gated ion channels. On-cell current-clamp recordings of olfactory receptor neurons from neonatal mouse slices revealed that ATP reduced cyclic nucleotide-induced electrical responses. These data also support the idea that ATP modulates odor sensitivity in mammalian olfactory neurons. Peripheral ATP-mediated odor suppression is a novel mechanism for reduced olfactory sensitivity during exposure to olfactotoxins and may be a novel neuroprotective mechanism.
机译：嘌呤能核苷酸，包括ATP和腺苷，是周围听觉和视觉感觉系统的重要神经调节剂（Thorne和Housley，1996）。有害刺激后，由嗅觉上皮（OE）释放的ATP为神经调节物质提供了生理来源，而与传出的神经支配无关。在这里，我们显示嘌呤能受体的多个亚型在嗅觉受体神经元和Sustentacular支持细胞中差异表达。嘌呤能受体的激活引起内向电流，并在培养的小鼠嗅觉受体神经元中增加细胞内钙。小鼠嗅觉上皮切片制备和共聚焦成像用于测量细胞内钙对气味，嘌呤能受体（P2R）激动剂或气味+ P2R激动剂的响应变化。药理研究表明，外源性和内源性ATP激活P2Y和P2X受体均显着降低了气味反应性。此外，嘌呤能受体拮抗剂增加了气味诱发的钙瞬变，提供直接证据表明内源性ATP通过激活嗅觉受体神经元中多种嘌呤能受体亚型来调节气味敏感性。 G蛋白偶联受体的异味激活导致cAMP产生增加，环状核苷酸门控通道的开放，Ca2 +和Na +的流入，膜的去极化以及电压门控和Ca2 +门控的离子通道的激活。新生小鼠切片中嗅觉受体神经元的细胞电流钳记录显示，ATP减少了环核苷酸诱导的电反应。这些数据也支持ATP调节哺乳动物嗅觉神经元的气味敏感性的想法。外围ATP介导的气味抑制是一种减少嗅觉毒素暴露过程中嗅觉敏感性降低的新机制，并且可能是一种新型的神经保护机制。

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