Traumatic brain injury in mice lacking the K channel, TREK-1.
作者： Khodadad Namiranian , Christa D Brink , Jerry Clay Goodman , Claudia S Robertson , Robert M Bryan
关键词: Hippocampus (mythology) 、 Endocrinology 、 Laser Doppler velocimetry 、 Neuroprotection 、 Traumatic brain injury 、 Internal medicine 、 Potassium channel 、 Cerebral cortex 、 Cortex (anatomy) 、 Anesthesia 、 Perfusion 、 Medicine
摘要: The purpose of this study was to determine whether the potassium channel, TREK-1, neuroprotective after traumatic brain injury (TBI). Since there are no selective blockers, we used TREK-1 knockout (KO) mice for our study. Wild-type (WT) and KO were anesthetized subjected controlled-cortical impact (deformation by 1.5 mm a 3-mm diameter rod traveling at 3 m/s). Laser Doppler perfusion (LDP) decreased ∼80% in injured cortex remained that level both WT (n=10 11, respectively). 50% 60% cortical areas directly adjacent site injury. There statistical differences LDP between genotype. contusion volume, determined 15 days TBI using hematoxylin eosin-stained coronal sections, 4.1±0.8 (n=10) 5.1±0.5 (n=11) mm(3) KO, respectively (not significant, P=0.34). Cell counts viable neurons CA1 CA3 regions hippocampus similar (P=0.51 0.84 CA3, We conclude expression does not provide protection TBI.
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