Kv1.3 in Microglia Cell Mediates Neurological Dysfunction after Traumatic Brain Injury

Abstract

Abstract Background Traumatic brain injury (TBI) is a kind of brain structure destruction and brain dysfunction syndrome caused by mechanical injury. At present, the treatment of traumatic brain injury is mainly neuroprotective drugs, but the efficacy is limited. Therefore, the exploration of effective therapeutic targets for traumatic brain injury has become a key scientific problem in current neuropharmacological research. Studies have found that neuroinflammation is closely related to the occurrence and development of traumatic brain injury. After activation of central microglia cell, various cellular inflammatory factors will be secreted, causing damage to the central nervous system and causing neuroinflammation. Studies have shown that potassium channel Kv1.3 plays a crucial role in microglia-mediated neuroinflammation, but the mechanism of microglial potassium channel Kv1.3 on traumatic brain injury remains unclear. Methods In this study, the functional localization of potassium channel Kv1.3 in microglia cell was investigated by behavioral observation, patch clamp, immunofluorescence, Western blotting, real-time PCR and other techniques in mice model of repetitive traumatic brain injury combined with Kv1.3 gene knockout mice. Results We found significant neurological deterioration in TBI mice, and knockdown of Kv1.3 effectively reversed TBI-mediated neurological dysfunction. The expression of inflammatory factors IL-1β and TNF-α was significantly increased in the hippocampus of mice with traumatic brain injury, and the down-regulation of Kv1.3 gene significantly inhibited the expression of these inflammatory factors. Conclusion Potassium channel Kv1.3 in microglia cell is an important regulatory target in repetitive traumatic brain injury.