کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4350235 | 1296978 | 2006 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Differential effect of glutamate transporter inhibition on EPSCs in the morphine naïve and morphine tolerant neonatal spinal cord slice
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Differential effect of glutamate transporter inhibition on EPSCs in the morphine naïve and morphine tolerant neonatal spinal cord slice Differential effect of glutamate transporter inhibition on EPSCs in the morphine naïve and morphine tolerant neonatal spinal cord slice](/preview/png/4350235.png)
چکیده انگلیسی
Opioid analgesic tolerance is a phenomenon defined as a need for increasingly higher doses of opiates to maintain suitable pain relief following repeated drug exposure. Research suggests that analgesic tolerance may result from heightened NMDA receptor (NMDAR) activity, but little is known regarding the mechanisms by which this elevated NMDAR activity develops. Recent evidence suggests that glutamate transporter down-regulation follows repeated opiate exposure and contributes to heightened pain sensitivity. Though glutamate transporter inhibition has been shown to increase activity of spinal cord neurons, it is unknown whether this increase contributes to the heightened NMDAR activity that underlies opiate tolerance. We directly tested this hypothesis by comparing the effects of glutamate transporter inhibition on excitatory post-synaptic currents (EPSCs) in the spinal cord dorsal horn of opiate naïve and opiate tolerant rats. We show that non-selective glutamate transporter inhibition increases the rate of spontaneous excitatory post-synaptic currents (sEPSCs) in the opiate naïve, but not opiate tolerant slice. This potentiation occurs in the presence of the sodium channel blocker tetrodotoxin (TTX) and is blocked by the NMDAR antagonist d-2-amino-5-phosphonovalerate (APV). The sEPSC rate is elevated at baseline in the opiate tolerant spinal cord slice compared to the opiate naïve slice, and glutamate transporter inhibition eliminates this difference. Taken together, we conclude that glutamate transporter inhibition directly contributes to heightened NMDAR activity. Furthermore, we propose that the increased neural activity observed in the opiate tolerant slice is due to a state of glutamate transporter down-regulation and resultant heightened NMDAR activity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 407, Issue 1, 16 October 2006, Pages 64-69
Journal: Neuroscience Letters - Volume 407, Issue 1, 16 October 2006, Pages 64-69
نویسندگان
Lisa M. Thomson, Jinsong Zeng, Gregory W. Terman,