R. Suzanne Zukin

TL;DR: An emerging concept is that activity-dependent, bidirectional regulation of NMDAR trafficking provides a dynamic and potentially powerful mechanism for the regulation of synaptic efficacy and remodelling, which, if dysregulated, can contribute to neuropsychiatric disorders such as cocaine addiction, Alzheimer's disease and schizophrenia.

TL;DR: Elevated mTOR signaling may provide a functional link between overactivation of group I mGluRs and aberrant synaptic plasticity in the fragile X mouse, mechanisms relevant to impaired cognition in fragile X syndrome.

TL;DR: It is demonstrated that PKC increases NMDA channel opening rate and delivers new NMDA channels to the plasma membrane through regulated exocytosis and regulates NMDAR channel gating and trafficking in recombinant systems and in neurons, mechanisms that may be relevant to synaptic plasticity.

TL;DR: This work shows that the Ca2+ permeability of neuronal NMDARs is under the control of the cyclic AMP–protein kinase A (cAMP-PKA) signaling cascade and provides a new mechanism whereby PKA regulates the induction of LTP.

TL;DR: Although not somatically heritable, epigenetic modifications in neurons are dynamic and reversible, which makes them good targets for therapeutic intervention, especially in neurodegenerative disorders and diseases.