Destabilization of neuronal calcium homeostasis by factors secreted from choroid plexus macrophage cultures in response to feline immunodeficiency virus
Destabilization of neuronal calcium homeostasis by factors secreted from choroid plexus macrophage cultures in response to feline immunodeficiency virus
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DOI：
10.1006/nbdi.2001.0459
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发表时间：
2002-03-01
影响因子：
6.1
通讯作者：
Meeker, RB
中科院分区：
文献类型：
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作者：
Bragg, DC;Boles, JC;Meeker, RB
脉络丛含有巨噬细胞的主要储存库，在被人类或猫免疫缺陷病毒 (FIV) 等慢病毒感染后，可有效地将病毒和神经毒素递送至大脑。然而，人们对它们对神经毒性的贡献知之甚少。将来自 FIV 感染的脉络丛巨噬细胞的培养基应用于培养的猫科动物皮质神经元，诱导了小幅急性钙升高，然后是延迟的钙失调（41％）或肿胀和破裂（23％）。 NMDA 谷氨酸受体阻断可防止急性钙增加，IP3 受体、电压门控钙通道和钠通道拮抗剂可抑制急性和晚期钙增加。在短暂接触谷氨酸后，对经过毒素处理的神经元的细胞内钙恢复进行分析，发现恢复的速度和程度有所下降。对细胞内钙不稳定的明显不同药理学贡献可能是由于巨噬细胞毒素干扰细胞内钙稳态恢复的能力。 (C) 2002 年爱思唯尔科学（美国）。
The choroid plexus contains a major reservoir of macrophages poised for efficient delivery of virus and neurotoxins to the brain after infection by lentiviruses such as human or feline immunodeficiency virus (FIV). However, their contribution to neurotoxicity is poorly understood. Medium from FIV-infected, choroid plexus macrophages applied to cultured feline cortical neurons induced a small acute calcium rise followed by either a delayed calcium deregulation (41%) or swelling and bursting (23%). NMDA glutamate receptor blockade prevented the acute calcium increase and antagonists to the IP3 receptor, voltage-gated calcium channels and sodium channels suppressed both the acute and late increases. Analysis of intracellular calcium recovery in toxin-treated neurons after a brief exposure to glutamate, revealed a decrease in the rate and extent of recovery. The apparent diverse pharmacological contributions to intracellular calcium destabilization may be due to the ability of macrophage toxins to interfere with recovery of intracellular calcium homeostasis. (C) 2002 Elsevier Science (USA).