BDNF-induced synaptic delivery of AMPAR subunits is differentially dependent on NMDA receptors and requires ERK.

摘要: Previous studies using an in vitro model of eyeblink classical conditioning turtles suggest that increased numbers synaptic AMPARs supports the acquisition and expression conditioned responses (CRs). Brain-derived neurotrophic factor (BDNF) its associated receptor tyrosine kinase, TrkB, is also required for CRs. Bath application BDNF alone induces delivery GluR1- GluR4-containing blocked by coapplication kinase inhibitor K252a. The molecular mechanisms involved BDNF-induced AMPAR trafficking remain largely unknown. aim this study was to determine whether incorporation utilizes similar cellular as occurs during conditioning. Using pharmacological blockade confocal imaging, results show GluR1 subunits or does not require activity NMDARs but mediated extracellular signal-regulated (ERK). In contrast, both NMDAR- well ERK-dependent. These findings indicate mimics observed activation some same intracellular signaling pathways a key signal transduction element postsynaptic events mediate