De‐palmitoylation by N‐(tert‐Butyl) hydroxylamine inhibits <scp>AMPAR</scp>‐mediated synaptic transmission via affecting receptor distribution in postsynaptic densities

Abstract

Our data suggest that the palmitoylation-deficient state initiated by NtBuHA preferentially reduces AMPAR function, which may potentially be used for the treatment of CNS disorders, especially infantile neuronal ceroid lipofuscinosis (Batten disease).