Persistence of learning-induced synapses depends on neurotrophic priming of glucocorticoid receptors.

ABSTRACT: Stress can either promote or impair learning and memory. Such opposing effects depend on whether synapses persist or decay after learning. Maintenance of new synapses formed at the time of learning upon neuronal network activation depends on the stress hormone-activated glucocorticoid receptor (GR) and neurotrophic factor release. Whether and how concurrent GR and neurotrophin signaling integrate to modulate synaptic plasticity and learning is not fully understood. Here, we show that deletion of the neurotrophin brain-derived neurotrophic factor (BDNF)-dependent GR-phosphorylation (PO₄) sites impairs long-term memory retention and maintenance of newly formed postsynaptic dendritic spines in the mouse cortex after motor skills training. Chronic stress and the BDNF polymorphism Va

SUBMITTER: Arango-Lievano M 

PROVIDER: S-EPMC6601006 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature