<p>In the mature central nervous system (CNS), γ-aminobutyric acid (GABA) and glycine (Gly) are predominant inhibitory neurotransmitters that negatively regulate neural activities. In contrast, GABA mediates membrane potential depolarization during development, and GABA/Gly become excitatory after nerve injury because of the high intracellular Cl⁻ concentration induced by low expression of K⁺, Cl⁻ cotransporter 2 (KCC2), which transports Cl⁻ out of neurons. Many studies have reported that during CNS development, GABAergic excitatory action might play crucial roles in neurogenesis through Ca²⁺ influx. Nevertheless, its involvement in neurogenesis has not been proven because the CNS can develop normally without GABAergic signals. Recently, two research groups demonstrated that low level of KCC2 (i.e., GABA/Gly excitation) after nerve injury is involved in axonal regeneration and in enhancement of functional recovery. In this manuscript, we review GABA/Gly excitation and introduce recent findings describing its involvement in axonal regeneration.</p>