Caffeine-mediated BDNF release regulates long-term synaptic plasticity through activation of IRS2 signaling.

ABSTRACT: Caffeine has cognitive-enhancing properties with effects on learning and memory, concentration, arousal and mood. These effects imply changes at circuital and synaptic level, but the mechanism by which caffeine modifies synaptic plasticity remains elusive. Here we report that caffeine, at concentrations representing moderate to high levels of consumption in humans, induces an NMDA receptor-independent form of LTP (_CAF LTP) in the CA1 region of the hippocampus by promoting calcium-dependent secretion of BDNF, which subsequently activates TrkB-mediated signaling required for the expression of _CAF LTP. Our data include the novel observation that insulin receptor substrate 2 (IRS2) is phosphorylated during induction of _CAF LTP, a process that requires cytosolic

SUBMITTER: Lao-Peregrin C 

PROVIDER: S-EPMC5697621 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature