The three isoforms of nitric oxide synthase distinctively affect mouse nocifensive behavior.

The three isoforms of nitric oxide synthase distinctively affect mouse nocifensive behavior.
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DOI:
10.1016/j.niox.2011.12.004
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发表时间:
2012-02-15
期刊:
Nitric oxide : biology and chemistry
影响因子:
--
通讯作者:
Quezado ZM
Quezado ZM
中科院分区:
其他
文献类型:
--
作者:
Finkel J;Guptill V;Khaibullina A;Spornick N;Vasconcelos O;Liewehr DJ;Steinberg SM;Quezado ZM

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一氧化氮合酶(NOSS)可调节炎症性和神经病理性疼痛中的热痛敏和机械过敏。然而,关于一氧化氮合酶对基础感觉神经纤维功能的影响,人们知之甚少。我们利用NOS1、NOS2和NOS3的遗传缺陷和药物抑制,通过测量5、250、2000赫兹电刺激的当前发声阈值来研究NOS1、NOS2和NOS3对基线发声行为的影响。电刺激优先刺激C、A、δ和Aβ纤维。与野生型相比,NOS1缺陷型动物对5、250和2000赫兹的反应具有显著更高的当前发声阈值。NOS2的遗传缺陷与对5赫兹(C-纤维)刺激反应较高的当前发声阈值有关。相比之下,与野生型动物相比,NOS3缺陷动物在5赫兹时的当前发声阈值较低,而在250赫兹和2000赫兹时的当前发声阈值显著降低。因此,一氧化氮合酶显著影响小鼠的基线发声阈值,并在电刺激感觉神经纤维的突触反应中发挥作用。
Nitric oxide synthases (NOSs) have been shown to modulate thermal hyperalgesia and mechanical hypersensitivity in inflammatory and neuropathic pain. However, little is known about the effect of NOSs on baseline function of sensory nerve fibers. Using genetic deficiency and pharmacologic inhibition of NOSs, we examined the impact of the three isoforms NOS1, NOS2, and NOS3 on baseline nocifensive behavior by measuring current vocalization threshold in response to electrical stimulation at 5, 250, 2000 Hz that preferentially stimulate C, Aδ, and Aβ fibers. In response to 5, 250 and 2000 Hz, NOS1-deficient animals had significantly higher current vocalization thresholds compared with wild-type. Genetic deficiency of NOS2 was associated with higher current vocalization thresholds in response to 5 Hz (C-fiber) stimulation. In contrast, NOS3-deficient animals had an overall weak trend toward lower current vocalization thresholds at 5 Hz and significantly lower current vocalization threshold compared with wild-type animals at 250 and 2000 Hz. Therefore, NOSs distinctively affect baseline mouse current vocalization threshold and appear to play a role on nocifensive response to electrical stimulation of sensory nerve fibers.
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