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Electrical stimulation of the posterior insula induces mechanical analgesia in a rodent model of neuropathic pain by modulating GABAergic signaling and activity in the pain circuitry
Brain Research ( IF 2.9 ) Pub Date : 2021-01-02 , DOI: 10.1016/j.brainres.2020.147237
Heloísa Alonso-Matielo 1 , Elizamara S Gonçalves 1 , Mariana Campos 1 , Victória R S Oliveira 1 , Elaine F Toniolo 2 , Adilson S Alves 3 , Ivo Lebrun 4 , Daniel C de Andrade 5 , Manoel J Teixeira 6 , Luiz R G Britto 3 , Clement Hamani 7 , Camila S Dale 8
Affiliation  

The insula has emerged as a critical target for electrical stimulation since it influences pathological pain states. We investigated the effects of repetitive electrical stimulation of the insular cortex (ESI) on mechanical nociception, and general locomotor activity in rats subjected to chronic constriction injury (CCI) of the sciatic nerve. We also studied neuroplastic changes in central pain areas and the involvement of GABAergic signaling on ESI effects. CCI rats had electrodes implanted in the left agranular posterior insular cortex (pIC), and mechanical sensitivity was evaluated before and after one or five daily consecutive ESIs (15 min each, 60 Hz, 210 μs, 1 V). Five ESIs (repetitive ESI) induced sustained mechanical antinociception from the first to the last behavioral assessment without interfering with locomotor activity. A marked increase in Fos immunoreactivity in pIC and a decrease in the anterior and mid-cingulate cortex, periaqueductal gray and hippocampus were noticed after five ESIs. The intrathecal administration of the GABAA receptor antagonist bicuculline methiodide reversed the stimulation-induced antinociception after five ESIs. ESI increased GAD65 levels in pIC but did not interfere with GABA, glutamate or glycine levels. No changes in GFAP immunoreactivity were found in this work. Altogether, the results indicate the efficacy of repetitive ESI for the treatment of experimental neuropathic pain and suggest a potential influence of pIC in regulating pain pathways partially through modulating GABAergic signaling.



中文翻译:

后脑岛的电刺激通过调节疼痛回路中的 GABA 能信号和活动,在啮齿动物神经性疼痛模型中诱导机械镇痛

脑岛已成为电刺激的关键目标,因为它会影响病理性疼痛状态。我们研究了岛叶皮层 (ESI) 重复电刺激对坐骨神经慢性收缩损伤 (CCI) 大鼠机械伤害感受和一般运动活动的影响。我们还研究了中枢疼痛区域的神经可塑性变化以及 GABA 能信号对 ESI 效应的影响。CCI 大鼠将电极植入左侧无颗粒后岛叶皮层 (pIC),并在每天连续 1 次或 5 次 ESI(每次 15 分钟,60 Hz,210 μs,1 V)前后评估机械敏感性。从第一次到最后一次行为评估,五个 ESI(重复性 ESI)在不干扰运动活动的情况下诱导持续的机械镇痛。在五次 ESI 后注意到 pIC 中 Fos 免疫反应性的显着增加以及前扣带回皮层和中扣带皮层、导水管周围灰质和海马体的减少。GABA 鞘内给药一个受体拮抗剂荷包牡丹碘化物经过五年的ESI逆转的刺激诱发的镇痛作用。ESI 增加了 pIC 中的 GAD65 水平,但不干扰 GABA、谷氨酸或甘氨酸水平。在这项工作中没有发现 GFAP 免疫反应性的变化。总之,结果表明重复 ESI 对治疗实验性神经性疼痛的疗效,并表明 pIC 在部分通过调节 GABA 能信号传导调节疼痛通路中的潜在影响。

更新日期:2021-01-02
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