title: Alteration in rectification of potassium channels in perinatal hypoxia ischemia brain damage.
abstract: Oligodendrocyte progenitor cells (OPCs) are susceptible to perinatal hypoxia ischemia brain damage (HIBD), which results in infant cerebral palsy due to the effects on myelination. The origin of OPC vulnerability in HIBD, however, remains controversial. In this study, we defined the HIBD punctate lesions by MRI diffuse excessive high signal intensity (DEHSI) in postnatal 7-day-old rats. The electrophysiological functional properties of OPCs in HIBD were recorded by patch-clamp in acute cerebral cortex slices. The slices were intracellularly injected with Lucifer yellow and immunohistochemically labeled with NG2 antibody to identify local OPCs. Passive membrane properties and K(+) channel functions in OPCs were analyzed to estimate the onset of vulnerability in HIBD. The resting membrane potential, membrane resistance, and membrane capacitance of OPCs were increased in both the gray and white matter of the cerebral cortex. OPCs in both the gray and white matter exhibited voltage-dependent K(+) currents, which consisted of the initiated rectified potassium currents (IA) and the sustained rectified currents (IK). The significant alternation in membrane resistance was influenced by the diversity of potassium channel kinetics. These findings suggest that the rectification of IA and IK channels may play a significant role in OPC vulnerability in HIBD.
authors.affiliation: Department of Neurobiology, The Third Military Medical University, Chongqing, China; and chenpenghui@tmmu.edu.cn.
authors.forename: Penghui
authors.initials: P
authors.lastname: Chen
authors.affiliation: Department of Pediatrics, Xinqiao Hospital, The Third Military Medical University, Chongqing, China.
authors.forename: Liyan
authors.initials: L
authors.lastname: Wang
authors.affiliation: Department of Neurobiology, The Third Military Medical University, Chongqing, China; and.
authors.forename: Qiyue
authors.initials: Q
authors.lastname: Deng
authors.affiliation: Department of Neurobiology, The Third Military Medical University, Chongqing, China; and.
authors.forename: Huaizhen
authors.initials: H
authors.lastname: Ruan
authors.affiliation: Department of Neurobiology, The Third Military Medical University, Chongqing, China; and.
authors.forename: Wenqin
authors.initials: W
authors.lastname: Cai
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002462:Cell Membrane / Q000502:physiology; D002540:Cerebral Cortex / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D025802:Electric Capacitance; D005260:Female; D020925:Hypoxia-Ischemia, Brain / Q000473:pathology / Q000503:physiopathology*; D007700:Kinetics; D008279:Magnetic Resonance Imaging; D008297:Male; D058953:Neural Stem Cells / Q000473:pathology / Q000502:physiology*; D009474:Neurons / Q000473:pathology / Q000502:physiology*; D009836:Oligodendroglia / Q000473:pathology / Q000502:physiology*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000378:metabolism*; D017207:Rats, Sprague-Dawley; D046509:Tissue Culture Techniques
chemical_list: D015221:Potassium Channels
keywords: NG2; hypoxia ischemia brain damage (HIBD); oligodendrocyte progenitor cell (OPC); potassium channel; rectification