کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6277859 | 1295775 | 2009 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Effects of activation of group III metabotropic glutamate receptors on spinal synaptic transmission in a rat model of neuropathic pain
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کلمات کلیدی
GDP-β-SIPSCmEPSC(RS)-α-cyclopropyl-4-phosphonophenylglycinemGluRsevoked excitatory postsynaptic currentCPPGeEPSCsmIPSCl-AP46-Cyano-7-nitroquinoxaline-2,3-dione - 6-Cyano-7-nitroquinoxaline-2،3-dioneguanosine 5′-O-(2-thiodiphosphate) - guanosine 5'-O- (2-thiodiphosphate)sIPSC - Şipscaminiature inhibitory postsynaptic current - جریان ممانعت کننده پستانیپتیک مینیاتوریinhibitory postsynaptic current - جریان پستانیپتیک مهارکنندهSpontaneous inhibitory postsynaptic current - جریان پستانیپتیک مهارکننده خود به خودیminiature excitatory postsynaptic current - جریان پستیینپتیک مضر تحریک آمیزCNQX - سیانکیوایکسMetabotropic glutamate receptors - گیرنده های متابوتروپیک گلوتامات
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Chronic neuropathic pain remains an unmet clinical problem because it is often resistant to conventional analgesics. Metabotropic glutamate receptors (mGluRs) are involved in nociceptive processing at the spinal level, but their functions in neuropathic pain are not fully known. In this study, we investigated the role of group III mGluRs in the control of spinal excitatory and inhibitory synaptic transmission in a rat model of neuropathic pain induced by L5/L6 spinal nerve ligation. Whole-cell recording of lamina II neurons was performed in spinal cord slices from control and nerve-ligated rats. The baseline amplitude of glutamatergic EPSCs evoked from primary afferents was significantly larger in nerve-injured rats than in control rats. However, the baseline frequency of GABAergic and glycinergic inhibitory postsynaptic currents (IPSCs) was much lower in nerve-injured rats than in control rats. The group III mGluR agonist l(+)-2-amino-4-phosphonbutyric acid (l-AP4) produced a greater inhibition of the amplitude of monosynaptic and polysynaptic evoked EPSCs in nerve-injured rats than in control rats. l-AP4 inhibited the frequency of miniature EPSCs in 66.7% of neurons in control rats but its inhibitory effect was observed in all neurons tested in nerve-injured rats. Furthermore, l-AP4 similarly inhibited the frequency of GABAergic and glycinergic IPSCs in control and nerve-injured rats. Our study suggests that spinal nerve injury augments glutamatergic input from primary afferents but decreases GABAergic and glycinergic input to spinal dorsal horn neurons. Activation of group III mGluRs attenuates glutamatergic input from primary afferents in nerve-injured rats, which could explain the antinociceptive effect of group III mGluR agonists on neuropathic pain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 158, Issue 2, 23 January 2009, Pages 875-884
Journal: Neuroscience - Volume 158, Issue 2, 23 January 2009, Pages 875-884
نویسندگان
H.-M. Zhang, S.-R. Chen, H.-L. Pan,