کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8837826 | 1612889 | 2018 | 38 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Electrical stimulation of the insular cortex as a novel target for the relief of refractory pain: An experimental approach in rodents
ترجمه فارسی عنوان
تحریک الکتریکی قشر ساحلی به عنوان یک هدف جدید برای تسکین درد مقاوم: یک روش تجربی در جوندگان
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کلمات کلیدی
ESITMSCCIPAGCB1S.E.M.AICMORchronic constriction injury - آسیب زدگی مزمنCES - اینCortical electrical stimulation - تحریک الکتریکی قشرdeep brain stimulation - تحریک عمقی مغزTranscranial magnetic stimulation - تحریک مغناطیسی مغزInteroception - تعاملinsula - جزیرهstandard error of the mean - خطای استاندارد میانگینNeuropathic pain - درد نوروپاتیکAntinociception - ضد انعقادAgranular insular cortex - قشر ساحلی AgranularNeuromodulation - نورومدولاسیون type 1 cannabinoid receptor - نوع 1 گیرنده کانابینوئیدNEP - نپMu opioid receptor - گیرنده اپیدمی م
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب رفتاری
چکیده انگلیسی
Cortical electrical stimulation (CES) has shown to be an effective therapeutic alternative for neuropathic pain refractory to pharmacological treatment. The primary motor cortex(M1) was the main cortical target used in the vast majority of both invasive and non-invasive studies. Despite positive results M1-based approaches still fail to relieve pain in a significant proportion of individuals. It has been advocated that the direct stimulation of cortical areas directly implicated in the central integration of pain could increase the efficacy of analgesic brain stimulation. Here, we evaluated the behavioral effects of electrical stimulation of the insular cortex (ESI) on pain sensitivity in an experimental rat model of peripheral neuropathy, and have described the pathways involved. Animals underwent chronic constriction of the sciatic nerve in the right hind limb and had concentric electrodes implanted in the posterior dysranular insular cortex. Mechanical nociception responses were evaluated before and at the end of a 15-min session of ESI (60 Hz, 210 μs, 1 V). ESI reversed mechanical hypersensitivity in the paw contralateral to the brain hemisphere stimulated, without inducing motor impairment in the open-field test. Pharmacological blockade of μ-opioid (MOR) or type 1-cannabinoid receptors (CB1R) abolished ESI-induced antinociceptive effects. Evaluation of CB1R and MOR spatial expression demonstrated differential modulation of CB1R and MOR in the periaqueductal gray matter (PAG) of ESI-treated rats in sub-areas involved in pain processing/modulation. These results indicate that ESI induces antinociception by functionally modulating opioid and cannabinoid systems in the PAG pain circuitry in rats with experimentally induced neuropathic pain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Behavioural Brain Research - Volume 346, 2 July 2018, Pages 86-95
Journal: Behavioural Brain Research - Volume 346, 2 July 2018, Pages 86-95
نویسندگان
Luiz Fabio Dimov, Elaine Flamia Toniolo, HeloÃsa Alonso-Matielo, Daniel Ciampi de Andrade, Luis Garcia-Larrea, Gerson Ballester, Manoel Jacobsen Teixeira, Camila Squarzoni Dale,