Does mTOR or NMDA receptor inhibition increase local dendritic synthesis of Kv1.1 channels in hippocampal neurons?
Synaptic excitation may cause local suppression of dendritic Kv1 channels by reducing their local synthesis via mTOR and NMDA receptor pathways.
Mammalian target of rapamycin (mTOR) is implicated in synaptic plasticity and local translation in dendrites. We found that the mTOR inhibitor, rapamycin, increased the Kv1.1 voltage-gated potassium channel protein in hippocampal neurons and promoted Kv1.1 surface expression on dendrites without altering its axonal expression. Moreover, endogenous Kv1.1 mRNA was detected in dendrites. Using Kv1.1 fused to the photoconvertible fluorescence protein Kaede as a reporter for local synthesis, we observed Kv1.1 synthesis in dendrites upon inhibition of mTOR or the N-methyl-d-aspartate (NMDA) glutamate receptor. Thus, synaptic excitation may cause local suppression of dendritic Kv1 channels by reducing their local synthesis.
Raab‐Graham et al. (Thu,) studied this question.