Restoration of gamma-aminobutyric acid homeostasis: A novel approach to alleviating central nervous system injury-associated immunodepression syndrome.

Injuries to the central nervous system can disrupt body functions and often cause excessive sympathetic activity, leading to immune suppression known as central nervous system injury-associated immunodepression syndrome. The connection between central nervous system injury and central nervous system injury-associated immunodepression syndrome is not fully clear. Gamma-aminobutyric acid, an important inhibitory neurotransmitter, helps excitation-inhibition balance in the nervous system, especially after spinal cord injuries. Impaired gamma-aminobutyric acid signaling causes an excitation-inhibition imbalance, which worsens neural plasticity, increases sympathetic overactivity, and may lead to central nervous system injury-associated immunodepression syndrome. This review discusses the roles of gamma-aminobutyric acid in protecting central nervous system structure and function and how its dysfunction contributes to abnormal plasticity and heightened reflexes. We also explore new treatments aimed at restoring gamma-aminobutyric acid balance, such as modulating potassium-chloride cotransporter 2, enhancing activity-dependent recovery, targeting microglial responses, and dietary approaches. Maintaining healthy gamma-aminobutyric acid activity is essential for preventing immune issues following central nervous system injury. This review emphasizes the regulation of gamma-aminobutyric acid as a promising target for future treatments of central nervous system injury-associated immunodepression syndrome.