有哪些信誉好的足球投注网站hiv-1gp120 induces neuronal apoptosis through enhancement of 4-aminopyridine-senstive outward k+ currentshiv-1gp120细胞凋亡神经元通过增强4-aminopyridine-senstive外k +电流.pdfVIP
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hiv-1gp120inducesneuronalapoptosisthroughenhancementof4-aminopyridine-senstiveoutwardkcurrentshiv-1gp120细胞凋亡神经元通过增强4-aminopyridine-senstive外k电流
HIV-1gp120 Induces Neuronal Apoptosis through Enhancement of 4-Aminopyridine-Senstive Outward K+ Currents 1,3 1 1 1 3 1,2 Lina Chen , Jianuo Liu , Changshui Xu , James Keblesh , Weijin Zang , Huangui Xiong * 1 Neurophysiology Laboratory, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America, 2 Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, United States of America, 3 Department of Pharmacology, College of Medicine, Xi’an Jiaotong University, Xi’an, People’s Republic of China Abstract Human immunodeficiency virus type 1 (HIV-1)-associated dementia (HAD) usually occurs late in the course of HIV-1 infection and the mechanisms underlying HAD pathogenesis are not well understood. Accumulating evidence indicates that neuronal voltage-gated potassium (Kv) channels play an important role in memory processes and acquired neuronal channelopathies in HAD. To examine whether Kv channels are involved in HIV-1-associated neuronal injury, we studied the effects of HIV-1 glycoprotein 120 (gp120) on outward K+ currents in rat cortical neuronal cultures using whole-cell patch techniques. Exposure of cortical neurons to gp120 produced a dose-dependent enhancement of A-type transient outward K+ currents (IA). The gp120-induced increase of IA was attenuated by T140, a specific antagonist for chemokine receptor CXCR4, suggesting gp120 enhancement of neuronal IA via CXCR4. Pretreatment of neuronal cultures with a protein kinase C (PKC) inhibitor, GF109203X, inhibited the gp120-induced increase of IA. Biological significance of gp120 enhancement of IA
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