INTACT NOCICEPTION-INDUCED NEUROPLASTICITY IN TRANSGENIC MICE DEFICIENT IN NEURONAL NITRIC-OXIDE SYNTHASE
INTACT NOCICEPTION-INDUCED NEUROPLASTICITY IN TRANSGENIC MICE DEFICIENT IN NEURONAL NITRIC-OXIDE SYNTHASE
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DOI：
10.1016/0306-4522(95)00395-y
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发表时间：
1995-12-01
期刊：
影响因子：
3.3
通讯作者：
HUANG, PL
中科院分区：
文献类型：
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作者：
CROSBY, G;MAROTA, JJA;HUANG, PL
一氧化氮被认为在多种形式的使用依赖性突触可塑性中发挥重要作用，包括有害外周刺激后的突触可塑性。这表明，在缺乏一氧化氮合酶神经元形式的转基因动物中，伤害感觉诱导的神经可塑性的发展可能受到损害。我们使用福尔马林伤害感觉模型在野生型和一氧化氮合酶敲除小鼠中验证了这一假设。福尔马林诱导的伤害性行为在敲除小鼠中是完整的。此外，在野生型小鼠中，一氧化氮合酶抑制剂阻断了伤害感觉诱导的神经可塑性，但对基因敲除没有影响，而吸入气态镇痛性氧化亚氮则减轻了两种表型中神经可塑性变化的发展。这些数据表明，一氧化氮对伤害感觉诱导的神经可塑性的发展是充分的，但不是必需的。
Nitric oxide is thought to play an important role in multiple forms of use-dependent synaptic plasticity, including that which follows noxious peripheral stimulation. This suggests that development of nociception-induced neuroplasticity should be impaired in transgenic animals lacking the neuronal form of nitric oxide synthase. We used the formalin model of nociception to test this hypothesis in wild-type and nitric oxide synthase knockout mice. Formalin-induced nociceptive behavior was intact in the knockout mice. Furthermore, administration of a nitric oxide synthase inhibitor blocked nociception-induced neuroplasticity in wildtype mice but had no effect in the knockouts, whereas inhalation of the gaseous analgesic nitrous oxide attenuated development of neuroplastic changes in both phenotypes. These data indicate that nitric oxide is sufficient but not essential for development of nociception-induced neuroplasticity.