Recruitment of functional GABAA receptors to postsynaptic domains by insulin

摘要: Modification of synaptic strength in the mammalian central nervous system (CNS) occurs at both pre- and postsynaptic sites1,2. However, because receptors are likely to be saturated by released transmitter, an increase number active may a more efficient way strengthening efficacy3,4,5,6,7. But there has been no evidence for rapid recruitment neurotransmitter membrane CNS. Here we report that insulin causes type A γ-aminobutyric acid (GABAA) receptor, principal receptor mediates inhibition CNS8, translocate rapidly from intracellular compartment plasma transfected HEK 293 cells, this relocation requires β2 subunit GABAA receptor. In CNS neurons, increases expression on dendritic membranes. We found functional receptors, thereby increasing amplitude GABAA-receptor-mediated miniature inhibitory currents (mIPSCs) without altering their time course. These results provide membrane, suggesting fundamental mechanism generation plasticity.