Gabrb2, encoding the β2 subunit of the γ -aminobutyric acid type A (GABAA) receptor, is a crucial gene. GABAA receptors are the main inhibitory system in the central nervous system, involved in synaptogenesis, neurogenesis, and the regulation of neuronal plasticity and learning [1]. The GABRB2 gene is located on chromosome 5q34, and its encoded β2 subunit combines with α and γ subunits to form a major GABAA receptor subtype, accounting for 43% of all GABAA receptors in the mammalian brain [1].

Gabrb2 -knockout mice have provided valuable insights. These mice exhibit schizophrenia-like behavior, including prepulse inhibition (PPI) deficit, locomotor hyperactivity, and sociability impairments, along with neuroinflammation, which can be ameliorated by the antipsychotic drug risperidone [4]. They also show double-directed premenstrual dysphoric disorder (PMDD)-like symptoms, such as changes in anxiety-like and depression-like emotions, social, learning, and memory capacities, as well as neurotransmitter metabolism disturbance [3]. Additionally, the knockout mice display a range of epilepsy phenotypes, from genetic generalized epilepsy to developmental and epileptic encephalopathy, with 58% having pharmacoresistant epilepsy [2].

In conclusion, Gabrb2 plays an essential role in the central nervous system through its involvement in GABAA receptor formation. Studies using Gabrb2-knockout mouse models have revealed its significance in various neuropsychiatric disorders, including schizophrenia, PMDD, and epilepsy. Understanding Gabrb2's function can potentially lead to new therapeutic approaches for these diseases.