Acid-Ion Sensing Channel 1a Deletion Reduces Chronic Brain Damage and Neurological Deficits after Experimental Traumatic Brain Injury

• DOI: 10.1089/neu.2020.7568
• Publication Date: 2021-03-27T10:59:25Z
• Authors: Shiqi Cheng; Xiang Mao; Xiangjiang Lin; Antonia Wehn; Senbin Hu; Uta Mamrak; Igor Khalin; Maria Wostrack; Florian Ringel; Nikolaus Plesnila; Nicole A. Terpolilli
• Keywords: Brain damage; Acid-sensing ion channel

Traumatic brain injury (TBI) causes long-lasting neurodegeneration and cognitive impairments; however, the underlying mechanisms of these processes are not fully understood. Acid-sensing ion channels 1a (ASIC1a) voltage-gated Na+- Ca2+-channels shown to be involved in neuronal cell death; their role for chronic post-traumatic damage is largely unknown. To address this issue, we used ASIC1a-deficient mice investigated outcome up 6 months after TBI. wild-type (WT) littermates were subjected controlled cortical impact (CCI) or sham surgery. Brain water content was analyzed 24 h behavioral CCI. Lesion volume assessed longitudinally by magnetic resonance imaging histology. significantly reduced ASIC1a-/- animals compared WT controls. Over time, showed lesion hippocampal damage. This translated into improved function depression-like behavior. Microglial activation mice. In conclusion, ASIC1a deficiency resulted edema formation acutely TBI less damage, functional impairments, neuroinflammation injury. Hence, seems