Possible regulation by excitatory signals on GABAB receptor desensitization via AMPK activation.

GABA_B受体R2亚基上依赖于AMPK的磷酸化位点p783水平的升高抑制了受体的脱敏。在以DMEM为基础的培养液中培养的原代神经元中，NMDA暴露可增加p783的表达水平。另一方面，在体外体系中，根据AMPK活性的降低，磷酸化位点立即去磷酸化。因此，AMPK活性的变化可迅速调节GABA_B受体的功能。

The increase in the p783 level, which is AMPK-dependent phosphorylation site on GABA_B receptors R2 subunit, suppresses desensitization of the receptors. The p783 level was increased by NMDA exposure in the primary neurons, which were cultured in DMEM-based medium. On the other hand, the phosphorylation site immediately dephosphorylated in vitro system, according to the decrease in AMPK activity. It is thus suggested that GABA_B receptors functions were promptly regulated by the alteration of AMPK activity.