Localization of excitatory amino acid transporters EAAT1 and EAAT2 in human postmortem cortex: a light and electron microscopic study.

Localization of excitatory amino acid transporters EAAT1 and EAAT2 in human postmortem cortex: a light and electron microscopic study.
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DOI:
10.1016/j.neuroscience.2014.07.019
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发表时间:
2014-09-26
期刊:
影响因子:
3.3
通讯作者:
McCullumsmith, R. E.
McCullumsmith, R. E.
中科院分区:
医学3区
文献类型:
--
作者:
Roberts, R. C.;Roche, J. K.;McCullumsmith, R. E.

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The process of glutamate release, activity, and reuptake involves the astrocyte, the presynaptic and postsynaptic neuron. Glutamate is released into the synapse and may occupy and activate receptors on both neurons and astrocytes. Glutamate is rapidly removed from the synapse by a family of plasma membrane excitatory amino acid transporters (EAATs), also localized to neurons and astrocytes. The purpose of the present study was to examine EAAT labeling in postmortem human cortex at the light and electron microscopic levels. Postmortem prefrontal cortex was processed for EAAT1 and EAAT2 immunohistochemistry. At the light microscopic level, EAAT1 and EAAT2 labeling was found in both grey and white matter. Most cellular labeling was in small cells which were morphologically similar to glia. In addition, EAAT1 labeled neurons were scattered throughout, some of which were pyramidal in shape. At the electron microscopic level, EAAT1 and EAAT2 labeling was found in astrocytic soma and processes surrounding capillaries. EAAT labeling was also found in small astocytic processes adjacent to axon terminals forming asymmetric (glutamatergic) synapses. While EAAT2 labeling was most prevalent in astrocytic processes, EAAT1 labeling was also present in neuronal processes including the soma, axons, and dendritic spines. Expression of EAAT1 protein on neurons may be due to the hypoxia associated with the postmortem interval, and requires further confirmation. The localization of EAATs on the astrocytic plasma membrane and adjacent to excitatory synapses is consistent with the function of facilitating glutamate reuptake and limiting glutamate spillover. Establishment that EAAT1 and EAAT2 can be measured at the EM level in human postmortem tissues will permit testing of hypotheses related to these molecules in diseases lacking analogous animal models.
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