Chronic Stress and Lithium Treatments Alter Hippocampal Glutamate Uptake and Release in the Rat and Potentiate Necrotic Cellular Death After Oxygen and Glucose Deprivation
Chronic Stress and Lithium Treatments Alter Hippocampal Glutamate Uptake and Release in the Rat and Potentiate Necrotic Cellular Death After Oxygen and Glucose Deprivation
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DOI：
10.1007/s11064-011-0404-7
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发表时间：
2011-05-01
影响因子：
4.4
通讯作者：
Dalmaz, Carla
中科院分区：
文献类型：
--
作者：
de Vasconcellos-Bittencourt, Ana Paula S.;Vendite, Deusa Aparecida;Dalmaz, Carla
本研究旨在探讨慢性多元应激和锂离子治疗对大鼠海马谷氨酸能活性和神经元易损性的影响。雄性Wistar大鼠同时接受锂治疗，并在40天内进行慢性变量应激，然后通过切片和突触体测量海马谷氨酸能的摄取和释放。我们观察到锂处理大鼠突触体[H-3]谷氨酸摄取增加，海马[H-3]谷氨酸刺激释放增加。慢性应激增加突触体基底[H-3]谷氨酸释放，减少海马切片[H-3]谷氨酸摄取。在评估细胞脆弱性时，应激和锂都增加了氧和葡萄糖剥夺（OGD）后的细胞死亡。我们认为，应激对谷氨酸活性的影响可能是应激暴露后观察到的神经危害的部分原因，并且，尽管描述了锂的神经保护作用，但它增加了OGD后神经元的易损性。
This study was undertaken to evaluate the effects of chronic variate stress and lithium treatment on glutamatergic activity and neuronal vulnerability of rat hippocampus. Male Wistar rats were simultaneously treated with lithium and submitted to a chronic variate stress protocol during 40 days, and afterwards the hippocampal glutamatergic uptake and release, measured in slices and synaptosomes, were evaluated. We observed an increased synaptosomal [H-3]glutamate uptake and an increase in [H-3]glutamate stimulated release in hippocampus of lithium-treated rats. Chronic stress increased basal [H-3]glutamate release by synaptosomes, and decreased [H-3]glutamate uptake in hippocampal slices. When evaluating cellular vulnerability, both stress and lithium increased cellular death after oxygen and glucose deprivation (OGD). We suggest that the manipulation of glutamatergic activity induced by stress may be in part responsible for the neuroendangerment observed after stress exposure, and that, in spite of the described neuroprotective effects of lithium, it increased the neuronal vulnerability after OGD.