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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Blocking caspase activity prevents transsynaptic neuronal apoptosis and the loss of inhibition in lamina II of the dorsal horn after peripheral nerve injury.
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Blocking caspase activity prevents transsynaptic neuronal apoptosis and the loss of inhibition in lamina II of the dorsal horn after peripheral nerve injury.

机译：阻断半胱天冬酶活性可防止突触后神经元凋亡和周围神经损伤后背角lamina II的抑制作用丧失。

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摘要

We show that transsynaptic apoptosis is induced in the superficial dorsal horn (laminas I-III) of the spinal cord by three distinct partial peripheral nerve lesions: spared nerve injury, chronic constriction, and spinal nerve ligation. Ongoing activity in primary afferents of the injured nerve and glutamatergic transmission cause a caspase-dependent degeneration of dorsal horn neurons that is slow in onset and persists for several weeks. Four weeks after spared nerve injury, the cumulative loss of dorsal horn neurons, determined by stereological analysis, is >20%. GABAergic inhibitory interneurons are among the neurons lost, and a marked decrease in inhibitory postsynaptic currents of lamina II neurons coincides with the induction of apoptosis. Blocking apoptosis with the caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD) prevents the loss of GABAergic interneurons and the reduction of inhibitory currents. Partial peripheral nerve injury results in pain-like behavioral changes characterized by hypersensitivity to tactile or cold stimuli. Treatment with zVAD, which has no intrinsic analgesic properties, attenuates this neuropathic pain-like syndrome. Preventing nerve injury-induced apoptosis of dorsal horn neurons by blocking caspase activity maintains inhibitory transmission in lamina II and reduces pain hypersensitivity.
机译：我们表明，通过三个不同的部分周围神经病变在脊髓的浅背角（层I-III）中诱导跨突触细胞凋亡：幸免神经损伤，慢性收缩和脊髓神经结扎。受伤神经的初级传入活动的持续进行和谷氨酸能传递导致背角神经元的半胱天冬酶依赖性变性，其发作缓慢，持续数周。幸免的神经损伤后四周，通过体视学分析确定的背角神经元累积损失> 20％。 GABA能性抑制性神经元在丢失的神经元中，而层板II神经元的抑制性突触后电流的明显减少与细胞凋亡的诱导相吻合。用半胱天冬酶抑制剂苄氧基羰基-Val-Ala-Asp（OMe）-氟甲基酮（zVAD）阻止细胞凋亡，可防止GABA能中间神经元的丢失和抑制电流的减少。部分周围神经损伤导致类似疼痛的行为改变，其特征是对触觉或冷刺激过敏。 zVAD的治疗没有内在的镇痛作用，可减轻这种神经性疼痛样综合征。通过阻止caspase活性来防止神经损伤引起的背角神经元凋亡，可维持层板II中的抑制性传递并降低疼痛超敏性。

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