摘要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.