Spatial and temporal pattern of changes in the number of GAD65-immunoreactive inhibitory terminals in the rat superficial dorsal horn following peripheral nerve injury.
Spatial and temporal pattern of changes in the number of GAD65-immunoreactive inhibitory terminals in the rat superficial dorsal horn following peripheral nerve injury.
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DOI：
10.1186/1744-8069-10-57
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发表时间：
2014-09-04
期刊：
影响因子：
3.3
通讯作者：
Ribeiro-da-Silva A
中科院分区：
文献类型：
--
作者：
Lorenzo LE;Magnussen C;Bailey AL;St Louis M;De Koninck Y;Ribeiro-da-Silva A
抑制性中间神经元是脊髓背角回路的重要组成部分，在脊髓背角回路中，它们调节脊髓伤害性感受。现在有相当多的证据表明，脊髓背角抑制的减少有助于神经性疼痛。神经损伤后这些抑制性神经元的丢失是被提出来解释抑制减少的机制之一;然而，这仍然存在争议。这部分是因为以前的研究集中在抑制性神经元的全局测量上，而没有评估抑制性突触的数量。为了解决这一问题，我们进行了定量分析的抑制性终端的数量的空间和时间的变化，谷氨酸脱羧酶65（GAD 65）免疫反应性检测，在脊髓后角浅层慢性压迫性损伤（CCI）大鼠坐骨神经。Isolectin B4（IB 4）标记用于确定直接受周围神经损伤影响的背角内的位置。损伤后脊髓I、II层GAD 65抑制性终末密度降低。在LII中GAD 65终末的损失最大，最高下降发生在3-4周左右，并在56天部分恢复。GAD 65终端的数量的变化的时间过程相关性以及与IB 4标记的损失，并与机械和热刺激的阈值改变。我们对GAD 65+抑制性末端的详细分析清楚地表明，神经损伤引起GAD 65免疫反应性末端的短暂丧失，并表明这些改变可能参与疼痛行为的发展和改善。
Inhibitory interneurons are an important component of dorsal horn circuitry where they serve to modulate spinal nociception. There is now considerable evidence indicating that reduced inhibition in the spinal dorsal horn contributes to neuropathic pain. A loss of these inhibitory neurons after nerve injury is one of the mechanisms being proposed to account for reduced inhibition; however, this remains controversial. This is in part because previous studies have focused on global measurements of inhibitory neurons without assessing the number of inhibitory synapses. To address this, we conducted a quantitative analysis of the spatial and temporal changes in the number of inhibitory terminals, as detected by glutamic acid decarboxylase 65 (GAD65) immunoreactivity, in the superficial dorsal horn of the spinal cord following a chronic constriction injury (CCI) to the sciatic nerve in rats. Isolectin B4 (IB4) labelling was used to define the location within the dorsal horn directly affected by the injury to the peripheral nerve. The density of GAD65 inhibitory terminals was reduced in lamina I (LI) and lamina II (LII) of the spinal cord after injury. The loss of GAD65 terminals was greatest in LII with the highest drop occurring around 3–4 weeks and a partial recovery by 56 days. The time course of changes in the number of GAD65 terminals correlated well with both the loss of IB4 labeling and with the altered thresholds to mechanical and thermal stimuli. Our detailed analysis of GAD65+ inhibitory terminals clearly revealed that nerve injury induced a transient loss of GAD65 immunoreactive terminals and suggests a potential involvement for these alterations in the development and amelioration of pain behaviour.
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影响因子：
5.3
作者：
Lorenzo, Louis-Etienne;Godin, Antoine G.;De Koninck, Yves
通讯作者：
De Koninck, Yves
影响因子：
5.3
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Casals-Diaz, Laura;Vivo, Meritxell;Navarro, Xavier
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影响因子：
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影响因子：
16.2
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通讯作者：
TOBIN, AJ
影响因子：
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作者：
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通讯作者：
Plenderleith, MB