Plasticity in expression of the glutamate transporters GLT-1 and GLAST in spinal dorsal horn glial cells following partial sciatic nerve ligation.
Plasticity in expression of the glutamate transporters GLT-1 and GLAST in spinal dorsal horn glial cells following partial sciatic nerve ligation.
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部分坐骨神经结扎后,谷氨酸转运蛋白表达的可塑性和脊柱背角胶质细胞中的胶状。
DOI:
10.1186/1744-8069-5-15
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发表时间:
2009-03-26
期刊:
影响因子:
3.3
通讯作者:
Dougherty PM
中科院分区:
文献类型:
--
作者:
Xin WJ;Weng HR;Dougherty PM
Clearance of synaptically released glutamate, and hence termination of glutamatergic neurotransmission, is carried out by glutamate transporters, most especially glutamate transporter-1 (GLT-1) and the glutamate-aspartate transporter (GLAST) that are located in astrocytes. It is becoming increasingly well appreciated that changes in the function and expression of GLT-1 and GLAST occur under different physiological and pathological conditions. Here we investigated the plasticity in expression of GLT-1 and GLAST in the spinal dorsal horn using immunohistochemistry following partial sciatic nerve ligation (PSNL) in rats. Animals were confirmed to develop hypersensitivity to mechanical stimulation by 7 days following PSNL. Baseline expression of GLT-1 and GLAST in naive animals was only observed in astrocytes and not in either microglia or neurons. Microglia and astrocytes showed evidence of reactivity to the nerve injury when assessed at 7 and 14 days following PSNL evidenced by increased expression of OX-42 and GFAP, respectively. In contrast, the total level of GLT-1 and GLAST protein decreased at both 7 and 14 days after PSNL. Importantly, the cellular location of GLT-1 and GLAST was also altered in response to nerve injury. Whereas activated astrocytes showed a marked decrease in expression of GLT-1 and GLAST, activated microglia showed de novo expression of GLT-1 and GLAST at 7 days after PSNL and this was maintained through day 14. Neurons showed no expression of GLT-1 or GLAST at any time point. These results indicate that the expression of glutamate transporters in astrocytes and microglia are differentially regulated following nerve injury.
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影响因子:
3.3
作者:
Maeda S;Kawamoto A;Yatani Y;Shirakawa H;Nakagawa T;Kaneko S
通讯作者:
Kaneko S
影响因子:
7.4
作者:
Ma, WY;Quirion, R
通讯作者:
Quirion, R
影响因子:
7.4
作者:
SELTZER, Z;DUBNER, R;SHIR, Y
通讯作者:
SHIR, Y
影响因子:
7.4
作者:
Liaw, WJ;Stephens, RL;Tao, YX
通讯作者:
Tao, YX
影响因子:
2.9
作者:
Cata, Juan P.;Weng, Han-Rong;Dougherty, Patrick M.
通讯作者:
Dougherty, Patrick M.