γ-Aminobutyric acid (GABA) is a major inhibitory transmitter in the mammalian central nervous system (CNS), which exerts a powerful influence on neuronal network activity.  Changing GABA-ergic transmission leads to significant changes in CNS function.  GABA has been implicated in several CNS functions and disorders; therefore it is important to understand plasticity of GABA-ergic pathways.  GABA seems to be excitatory in neonates but inhibitory in adult animals.  High-frequency activation in neonatal rat brain switches GABA from being excitatory to being inhibitory.  While GABA-ergic plasticity occurs in neonates and adults, there are differences in mechanisms.  Moreover, different types of plasticity have been reported (short- vs. long- term; potentiation vs. depression, etc.) with differing mechanisms. In neonatal rat hippocampus, a Ca²⁺-dependent long-term potentiation (LTP) is described, while in adult rats, LTP in the hippocampal CA1 area is independent of postsynaptic Ca²⁺ and doesn’t require N-methyl-D-aspartate (NMDA) receptor-activation, but LTP in the deep cerebellar nuclei (DCN) seems to require both.  Endogenous benzodiazepine agonists seem to be involved in LTP in the CA1 area. Long-term depression (LTD) has been described in the DCN and it is dependent on post-synaptic Ca²⁺ and the activation of NMDA receptors and protein phosphatases.  GABA-ergic plasticity also occurs in the cerebellar cortex.  In conclusion, GABA-ergic plasticity of different types is described in literature.  Age- and region- dependent differences as well as different mechanisms of plasticity exist. GABA-ergic plasticity must be taken into consideration for a better understanding of CNS physiology, CNS disorders and for therapeutic strategies.