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GABA is the predominant inhibitory neurotransmitter in the adult brain.Deficiency of GABAergic neurotrans-mission may be involved in serious neurological disorders,including epilepsy,anxiety,depression,and schizophrenia.Despite the vital function of GABA in the brain,the molecular mechanism of GABAergic synapse formation is still largely unclear.We have employed primary neuronal cultures to study the presynaptic and postsynaptic differentiation during GABAergic synaptogenesis.We found that GABAergic postsynaptic assembly is a very rapid process,much faster than its counterpart presynaptic assembly in cultured embryonic neurons.To understand why it is so rapidly assembled,we used heterologous expression system HEK293 cells to study the essential molecular composition of GABAergic postsynaptic apparatus.We demonstrate that besides GABAA receptors,which is necessary to detect GABA transmitter,the only molecule needed is a cell adhesion molecule neuroligin-2 to build a fully functional GABAergic postsynaptic apparatus.