Viral infection of developing GABAergic neurons in a model of hippocampal disinhibition
Viral infection of developing GABAergic neurons in a model of hippocampal disinhibition
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DOI：
10.1097/00001756-200008030-00019
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发表时间：
2000-08-03
期刊：
影响因子：
1.7
通讯作者：
Miller, AH
中科院分区：
文献类型：
--
作者：
Pearce, BD;Valadi, NM;Miller, AH
围产期病毒感染可破坏海马发育并导致选择性神经元死亡的机制可能与颞叶癫痫和精神分裂症有关。尽管在这些疾病中抑制性中间神经元异常，但这种神经递质变化与病毒感染之间的因果关系仍不清楚。这种关系进行了检查，在一个模型中，大鼠，感染淋巴细胞性脉络丛脑膜炎病毒（LCMV）作为新生儿，表现出海马齿状颗粒细胞和神经元过度兴奋的逐渐丧失。目前的数据表明，GABA能中间神经元的LCMV抗原的双重免疫染色之前的损失的齿状颗粒细胞，支持的假设，LCMV可能会破坏发展中的抑制回路，导致不平衡的兴奋性神经传递和最终死亡的齿状颗粒细胞由于兴奋性毒性。NeuroReport 11：2433-2438（C）2000 Lippincott威廉姆斯和威尔金斯。
Mechanisms by which perinatal viral infections can disrupt hippocampal development and cause selective neuronal death may have implications for temporal lobe epilepsy and schizophrenia. Despite abnormalities of inhibitory interneurons in these diseases, the causal relationships between such neurotransmitter changes and viral infections remain unclear. This relationship was examined in a model in which rats, infected with lymphocytic choriomeningitis virus (LCMV) as neonates, manifest a gradual loss of hippocampal dentate granule cells and neuronal hyperexcitability. The current data demonstrate that GABAergic interneurons are dual immunostained for LCMV antigens prior to the loss of dentate granule cells, supporting the hypothesis that LCMV may disrupt developing inhibitory circuits causing unbalanced excitatory neurotransmission and the eventual death of dentate granule cells due to excitotoxicity. NeuroReport 11:2433-2438 (C) 2000 Lippincott Williams & Wilkins.