Brooke Sheila M, Sapolsky Robert M
Department of Biological Sciences, Gilbert Building Rm 432, Stanford University, Stanford, CA 94305-5020, USA.
Brain Res. 2003 May 16;972(1-2):137-41. doi: 10.1016/s0006-8993(03)02517-4.
Studies examining the development of AIDS Related Dementia have concentrated on neurotoxic properties of the HIV viral coat protein, gp120. We have previously shown that this neurotoxicity can be exacerbated by glucocorticoids (GCs), the stress hormones secreted by the adrenal. Moreover, GCs also worsen several of the mechanisms mediating gp120 neurotoxicity, such as increased calcium flux, ROS generation, and energy depletion. Gp120 interferes with the reuptake of glutamate in glia cultures, another possible mechanism by which it can be neurotoxic. This paper examines the role of GCs in exacerbating this phenomenon. It was found that while GCs do not exacerbate the decrease in reuptake of glutamate in glia cultures, they do enhance the decrease in mixed neuronal cultures and this latter effect appears to be energy-dependent.
研究艾滋病相关痴呆症发展的研究主要集中在HIV病毒包膜蛋白gp120的神经毒性特性上。我们之前已经表明，这种神经毒性会被糖皮质激素（GCs）加剧，糖皮质激素是肾上腺分泌的应激激素。此外，糖皮质激素还会使介导gp120神经毒性的几种机制恶化，如钙通量增加、活性氧生成和能量消耗。Gp120会干扰神经胶质细胞培养物中谷氨酸的再摄取，这是其产生神经毒性的另一种可能机制。本文研究了糖皮质激素在加剧这一现象中的作用。研究发现，虽然糖皮质激素不会加剧神经胶质细胞培养物中谷氨酸再摄取的减少，但它们确实会增强混合神经元培养物中谷氨酸再摄取的减少，而且后一种效应似乎依赖于能量。
