(H) Model of the receptor-specific regulation of AMPK-eEF2 signaling axis and their subsequent effect on global translation. mGluR stimulation (Left) inactivates AMPK, a necessity for the dephosphorylation of eEF2. This, in turn, leads to an enhanced protein synthesis thereby leading to the consumption of ATP. NMDAR stimulation (Right), however, led to an activation of AMPK by allowing the entry of extracellular Ca2+ through open NMDAR channels. This resulted in an increase in the eEF2 phosphorylation and an inhibition of global protein synthesis having no significant impact on neuronal energetics. 