| First Author | Namiranian K | Year | 2011 |
| Journal | J Cereb Blood Flow Metab | Volume | 31 |
| Issue | 3 | Pages | e1-6 |
| PubMed ID | 21157470 | Mgi Jnum | J:210797 |
| Mgi Id | MGI:5571838 | Doi | 10.1038/jcbfm.2010.223 |
| Citation | Namiranian K, et al. (2011) Traumatic brain injury in mice lacking the K channel, TREK-1. J Cereb Blood Flow Metab 31(3):e1-6 |
| abstractText | The purpose of this study was to determine whether the potassium channel, TREK-1, was 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 TREK-1 KO mice were anesthetized and subjected to controlled-cortical impact injury (deformation of the brain by 1.5 mm by a 3-mm diameter rod traveling at a 3 m/s). Laser Doppler perfusion (LDP) decreased by approximately 80% in the injured cortex and remained at that level in both WT and TREK-1 KO mice (n=10 and 11, respectively). Laser Doppler perfusion decreased by 50% to 60% in cortical areas directly adjacent to the site of injury. There were no statistical differences in LDP between genotype. The contusion volume, determined 15 days after the TBI using hematoxylin and eosin-stained coronal brain sections, was 4.1+/-0.8 (n=10) and 5.1+/-0.5 (n=11) mm(3) for WT and TREK-1 KO, respectively (not significant, P=0.34). Cell counts of viable neurons in the CA1 and CA3 regions of the hippocampus were similar between WT and TREK-1 KO mice (P=0.51 and 0.84 for CA1 and CA3, respectively). We conclude that TREK-1 expression does not provide brain protection after TBI. |
