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Urinary bladder hyporeflexia and reduced pain-related behaviour in P2X_3-deficient mice

机译：P2X_3缺陷小鼠的膀胱反射不足和疼痛相关行为减少

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Extracellular ATP is implicated in numerous sensory processes ranging from the response to pain to the regulation of motility in visceral organs. The ATP receptor P2X_3 is selectively expressed on small diameter sensory neurons, supporting this hypothesis. Here we show that mice deficient in P2X_3 lose the rapidly desensitizing ATP-induced currents in dorsal root ganglion neurons. P2X_3 deficiency also causes a reduction in the sustained ATP-induced currents in nodose ganglion neurons. P2X_3-null mice have reduced pain-related behaviour in response to injection of ATP and formalin. Significantly, P2X_3-null mice exhibit a marked urinary bladder hyporeflexia, characterized by decreased voiding frequency and increased bladder capacity, but normal bladder pressures. Immunohistochemical studies localize P2X_3 to nerve fibres innervating the urinary bladder of wild-type mice, and show that loss of P2X_3 does not alter sensory neuron innervation density. Thus, P2X_3 is critical for peripheral pain responses and afferent pathways controlling urinary bladder volume reflexes. Antagonists to P2X_3 may therefore have therapeutic potential in the treatment of disorders of urine storage and voiding such as overactive bladder.
机译：细胞外ATP涉及许多感觉过程，范围从对疼痛的反应到内脏器官运动性的调节。 ATP受体P2X_3在小直径感觉神经元上选择性表达，支持这一假设。在这里，我们显示缺乏P2X_3的小鼠失去了背根神经节神经元中快速脱敏ATP诱导的电流。 P2X_3缺乏症还导致结节神经节神经元中持续性ATP诱导的电流减少。 P2X_3-null小鼠因注射ATP和福尔马林而减少了与疼痛相关的行为。值得注意的是，P2X_3-null小鼠表现出明显的膀胱反射不足，其特征在于排尿频率降低和膀胱容量增加，但膀胱压力正常。免疫组织化学研究将P2X_3定位于神经纤维，神经纤维支配野生型小鼠的膀胱，并表明P2X_3的丧失不会改变感觉神经元的神经支配密度。因此，P2X_3对于周围疼痛反应和控制膀胱体积反射的传入途径至关重要。因此，P2X_3的拮抗剂可能具有治疗尿液储存和排尿障碍（如膀胱过度活动症）的潜力。

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