کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278055 | 1295791 | 2008 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Tactile allodynia can occur in the spared nerve injury model in the rat without selective loss of GABA or GABAA receptors from synapses in laminae I-II of the ipsilateral spinal dorsal horn
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کلمات کلیدی
TSApostembedding immunocytochemistrySNIVGATIB4IPSCCCIDABGADVIP3,3′-diaminobenzidine - 3،3'-diaminobenzidineEPSC - EPSCoRchronic constriction injury - آسیب زدگی مزمنSpared nerve injury - آسیب عصب آسیب دیدهisolectin B4 - ایزوکتین B4Antigen retrieval - بازیابی آنتیژنTyramide Signal Amplification - تقویت سیگنال تیرامیدTUNEL - تونلinhibitory postsynaptic current - جریان پستانیپتیک مهارکنندهexcitatory postsynaptic current - جریان پستیینپتیک تحریک کنندهvesicular GABA transporter - حامل ویسکوزر GABANeuropathic pain - درد نوروپاتیکdorsal horn - شاخ پشتیvasoactive intestinal peptide - پپتید روده روده ایGlutamate decarboxylase - گلوتامات دکربوکسیلاز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Although there is evidence that reduced inhibition in the spinal dorsal horn contributes to neuropathic pain, the mechanisms that underlie this are poorly understood. We have previously demonstrated that there is no loss of neurons from laminae I-III in the spared nerve injury (SNI) model [Polgár E, Hughes DI, Arham AZ, Todd AJ (2005) Loss of neurons from laminas I-III of the spinal dorsal horn is not required for development of tactile allodynia in the SNI model of neuropathic pain. J Neurosci 25:6658-6666]. In this study we investigated whether there was a difference between ipsilateral and contralateral sides in the levels of GABA, the vesicular GABA transporter (VGAT), or the β3 subunit of the GABAA receptor at synapses in the medial part of the superficial dorsal horn in this model. Tissue from rats that had undergone SNI 4 weeks previously was examined with an electron microscopic immunogold method to reveal GABA, following pre-embedding detection of GABAA β3 to allow identification of GABAergic terminals. Assessment of labeling for the GABAA β3 subunit and VGAT was performed by using immunofluorescence and confocal microscopy. We found no difference in the intensity of immunolabeling for any of these markers on the two sides of the superficial dorsal horn. These results suggest that there is no significant loss of GABAergic boutons from the denervated area after SNI (which is consistent with the finding that neuronal death does not occur in this model) and that there is no depletion of GABA or GABAA receptors at GABAergic synapses within this region. An alternative explanation for disinhibition after nerve injury is that it results from reduced excitatory drive to GABAergic dorsal horn neurons following loss of primary afferent input to these cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 156, Issue 1, 22 September 2008, Pages 193-202
Journal: Neuroscience - Volume 156, Issue 1, 22 September 2008, Pages 193-202
نویسندگان
E. Polgár, A.J. Todd,