Shaping plasticity: Alterations in glutamate transporter localization as a pathophysiological mechanism in severe mental illness
Shaping plasticity: Alterations in glutamate transporter localization as a pathophysiological mechanism in severe mental illness
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塑造可塑性:谷氨酸转运蛋白定位的改变作为严重精神疾病的病理生理机制
DOI:
10.1038/mp.2016.79
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发表时间:
2016
影响因子:
11
通讯作者:
J. Meador
中科院分区:
文献类型:
--
作者:
R. Mccullumsmith;S. O’Donovan;J. Drummond;F. Benesh;M. Simmons;R. Roberts;T. Lauriat;V. Haroutunian;J. Meador
A shift in glutamate transporter splice variant expression from astrocytes to neurons in schizophrenia. Autoradiogram (a) of in situ hybridization for EAAT2 (pan) mRNA in the human thalamus. The highlighted region is the mediodorsal nucleus of the thalamus. Nissl stain of a 20-μm tissue section (b) from the mediodorsal nucleus, x20 magnification. Relay neurons (large cells, big circles) and astrocytes (small cells, small circles) were identified based on morphology. Large and small cells were harvested from subjects with schizophrenia and control subjects using laser-capture microdissection. Expression of EAAT2 protein in relay neurons in schizophrenia was confirmed using dual immunofluorescence (c). The white arrows indicate cells double labeled for NeuN and EAAT2 (yellow). QPCR analysis (d) of excitatory amino-acid transporter EAAT2B transcripts isolated from enriched populations of astrocytes (small cells) and relay neurons (large cells). For more information on this topic, please refer to the article by McCullumsmith et al. on pages 823–830.