BACKGROUND:Many brain areas participate to supraspinal control of nociception. In these regions, few studies have investigated the role of glial cells in supraspinal plasticity and the effect of 7-day intrathecal nerve growth factor-like (BB14®, Blueprint Biotech, Milano, Italy) treatment. METHODS:In male Sprague-Dawley rats, we evaluated by immunohistochemistry the morphological and molecular rearrangement of neuroglial network occurring in several supraspinal brain regions involved in pain processing following spared nerve injury (SNI) of the sciatic nerve. In particular, the medial prefrontal cortex, the amygdala (Amy), the nucleus accumbens (Acb), the thalamus and the periaqueductal gray were analysed. RESULTS:Despite the modifications occurring in the dorsal horn of spinal cord following SNI, no significant changes in the Iba1 and glial fibrillary acidic protein (GFAP) expression were detected in all the analysed supraspinal regions, except for the Amy, showing a remarkable GFAP increase. Interestingly, neuropathic rats also displayed a significant increase of glial transporters (GTs) in all the supraspinal regions. Finally, the analysis of vesicular glutamate transporter 1 (vGLUT1) and vesicular gamma-aminobutyric acid (GABA) transporter (vGAT) expression revealed a significant enhancement of glutamatergic/GABAergic ratio in all selected brain regions of SNI animals, except for Acb. Both glial activation in the Amy and alteration of GTs and vGLUT/vGAT levels observed in neuropathic animals were largely reversed by BB14® treatment. CONCLUSIONS:All together, these data strengthen the role of supraspinal neuroglial network plasticity in the establishment of neuropathic pain syndrome. The hallmark is represented by the divergence between glial reaction confined to Amy and the widespread changes in the GT distribution and glutamate/GABA ratio detected in the other supraspinal region.

译文

背景:许多大脑区域参与了脊髓上的伤害感受控制。在这些地区,很少有研究调查神经胶质细胞在棘上棘可塑性中的作用以及7天鞘内神经生长因子样治疗的作用(BB14®,Blueprint Biotech,米兰,意大利)。
方法:在雄性Sprague-Dawley大鼠中,我们通过免疫组织化学方法评估了坐骨神经备用神经损伤(SNI)后参与疼痛处理的多个棘上大脑区域中神经胶质网络的形态和分子重排。特别地,分析了内侧前额叶皮层,杏仁核(Amy),伏隔核(Acb),丘脑和导水管周围的灰色。
结果:尽管SNI后脊髓背角发生了改变,但除Amy外,在所有分析的脊髓上区中,Iba1和神经胶质纤维酸性蛋白(GFAP)的表达均未检测到显着变化,显示GFAP显着增加。有趣的是,神经病变大鼠在所有棘上神经区也显示出神经胶质转运蛋白(GTs)的显着增加。最后,对囊泡谷氨酸转运蛋白1(vGLUT1)和囊泡γ-氨基丁酸(GABA)转运蛋白(vGAT)表达的分析显示,除Acb外,SNI动物所有选定大脑区域的谷氨酸能/ GABA能比均显着提高。在神经病动物中观察到的Amy中的神经胶质激活以及GTs和vGLUT / vGAT水平的改变都可以通过BB14®治疗大幅度逆转。
结论:这些数据加在一起增强了脊髓上神经胶质网络可塑性在建立神经性疼痛综合征中的作用。具有标志性的特征是仅限于Amy的神经胶质反应与在其他上棘突区域中检测到的GT分布和谷氨酸/ GABA比的广泛变化之间存在差异。

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