کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4338138 | 1614847 | 2013 | 9 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Early spread of hyperexcitability to caudal dorsal horn networks after a chemically-induced lesion of the rat spinal cord in vitro Early spread of hyperexcitability to caudal dorsal horn networks after a chemically-induced lesion of the rat spinal cord in vitro](/preview/png/4338138.png)
Hyperexcitability of dorsal horn neurons has been shown to play a key role in neuropathic pain following chronic experimental spinal cord injury. With a neonatal in vitro spinal cord injury model, we show that a chemically-induced lesion leads to rapid gain-of-function of sublesional dorsal horn networks biased to hyperexcitation. The expression of the GABA synthetic enzyme GAD65 was significantly reduced at the same level of the spinal cord, suggesting a compromised inhibitory system. We propose that our model could be useful to test early approaches to contrast spinal cord injury-induced central sensitization of dorsal horn circuits.
► Chemically-induced spinal lesion evokes wide-spread dorsal root depolarization.
► Dorsal horns remote from the spinal lesion show early hyperexcitability.
► Remote segments show the impaired expression of GABA synthetic enzyme.
Journal: Neuroscience - Volume 229, 15 January 2013, Pages 155–163