The expression of kainate receptor subunits in hippocampal astrocytes after experimentally induced status epilepticus.
The expression of kainate receptor subunits in hippocampal astrocytes after experimentally induced status epilepticus.
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DOI：
10.1097/nen.0b013e3182a4b266
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发表时间：
2013-10
影响因子：
3.2
通讯作者：
Wilcox KS
中科院分区：
文献类型：
--
作者：
Vargas JR;Takahashi DK;Thomson KE;Wilcox KS
星形胶质细胞已成为突触传递的积极参与者，并越来越多地参与神经系统疾病，包括癫痫。成人胶质细胞酸性蛋白（GFAP）阳性海马星形胶质细胞在基础条件下的离子型谷氨酸受体表达是未知的。使用颞叶癫痫的化学惊厥持续状态（SE）模型，我们通过免疫组织化学和共定位分析表明，反应性海马星形胶质细胞表达红藻氨酸受体（KAR）亚单位后SE。在CA 1区，GluK 1，GluK 2/3，GluK 4，和GluK 5亚基表达GFAP阳性星形胶质细胞在癫痫发作免费或“潜伏”期SE后1周。在SE后8周，即SE后自发行为癫痫发作发生的时间，GluK 1和GluK 5亚基仍以显著水平表达。KAR亚单位的表达被发现在海马和周围皮质的星形胶质细胞，但没有在纹状体，嗅球，或脑干的GFAP阳性星形胶质细胞。为了更广泛地研究海马KAR表达，从解剖的海马中制备星形胶质细胞富集的组织组分，发现SE后比对照组具有更高的GluK 4表达。这些结果表明，星形胶质细胞开始表达KAR癫痫活动后，并建议他们的表达可能有助于癫痫的病理生理。
Astrocytes have emerged as active participants of synaptic transmission and are increasingly implicated in neurological disorders including epilepsy. Adult glial fibrillary acidic protein (GFAP)-positive hippocampal astrocytes are not known for ionotropic glutamate receptor expression under basal conditions. Using a chemoconvulsive status epilepticus (SE) model of temporal lobe epilepsy, we show by immunohistochemistry and colocalization analysis that reactive hippocampal astrocytes express kainate receptor (KAR) subunits following SE. In the CA1 region, GluK1, GluK2/3, GluK4, and GluK5 subunit expression was observed in GFAP-positive astrocytes during the seizure free or “latent” period 1 week following SE. At 8 weeks following SE, a time following SE when spontaneous behavioral seizures occur, the GluK1 and GluK5 subunits remained expressed at significant levels. KAR subunit expression was found in astrocytes in the hippocampus and surrounding cortex, but not in GFAP-positive astrocytes of striatum, olfactory bulb, or brainstem. To examine hippocampal KAR expression more broadly, astroglial-enriched tissue fractions were prepared from dissected hippocampi and were found to have greater GluK4 expression following SE than controls. These results demonstrate that astrocytes begin to express KARs following seizure activity and suggest that their expression may contribute to the pathophysiology of epilepsy.