Antidepressant actions of ketamine engage cell-specific translation via eIF4E

[1]  M. Picciotto,et al.  GABA interneurons are the cellular trigger for ketamine's rapid antidepressant actions. , 2019, The Journal of clinical investigation.

[2]  Mitchell H. Murdock,et al.  Sustained rescue of prefrontal circuit dysfunction by antidepressant-induced spine formation , 2019, Science.

[3]  J. Krystal,et al.  Altered Connectivity in Depression: GABA and Glutamate Neurotransmitter Deficits and Reversal by Novel Treatments , 2019, Neuron.

[4]  S. Southwick,et al.  Rapamycin, an Immunosuppressant and mTORC1 Inhibitor, Triples the Antidepressant Response Rate of Ketamine at 2 Weeks Following Treatment: A double-blind, placebo-controlled, cross-over, randomized clinical trial , 2018 .

[5]  R. Duman,et al.  Activity-dependent brain-derived neurotrophic factor signaling is required for the antidepressant actions of (2R,6R)-hydroxynorketamine , 2018, Proceedings of the National Academy of Sciences.

[6]  C. S. Lai,et al.  Ketamine and selective activation of parvalbumin interneurons inhibit stress-induced dendritic spine elimination , 2018, Translational Psychiatry.

[7]  L. McMahon,et al.  Disinhibition of CA1 pyramidal cells by low-dose ketamine and other antagonists with rapid antidepressant efficacy , 2018, Proceedings of the National Academy of Sciences.

[8]  Hailan Hu,et al.  Ketamine blocks bursting in the lateral habenula to rapidly relieve depression , 2018, Nature.

[9]  Nils Grabole,et al.  Genome-wide translating mRNA analysis following ketamine reveals novel targets for antidepressant treatment , 2018, bioRxiv.

[10]  K. Rosenblum,et al.  Calcium/Calmodulin-Dependent Protein Kinase II and Eukaryotic Elongation Factor 2 Kinase Pathways Mediate the Antidepressant Action of Ketamine , 2017, Biological Psychiatry.

[11]  K. Raab-Graham,et al.  Engaging homeostatic plasticity to treat depression , 2018, Molecular Psychiatry.

[12]  E. Kavalali,et al.  The Ketamine Metabolite 2R,6R-Hydroxynorketamine Blocks NMDA Receptors and Impacts Downstream Signaling Linked to Antidepressant Effects , 2018, Neuropsychopharmacology.

[13]  E. Kavalali,et al.  Effects of a ketamine metabolite on synaptic NMDAR function , 2017, Nature.

[14]  David M. Sabatini,et al.  mTOR Signaling in Growth, Metabolism, and Disease , 2017, Cell.

[15]  D. Sabatini,et al.  mTOR Signaling in Growth, Metabolism, and Disease , 2017, Cell.

[16]  C. Zarate,et al.  Ketamine: translating mechanistic discoveries into the next generation of glutamate modulators for mood disorders , 2017, Molecular Psychiatry.

[17]  Xi-Ping Huang,et al.  NMDAR inhibition-independent antidepressant actions of ketamine metabolites , 2016, Nature.

[18]  Oliver H. Miller,et al.  Two cellular hypotheses explaining the initiation of ketamine's antidepressant actions: Direct inhibition and disinhibition , 2016, Neuropharmacology.

[19]  D. Charney,et al.  A Randomized Controlled Trial of Intranasal Ketamine in Major Depressive Disorder , 2014, Biological Psychiatry.

[20]  M. Bernier,et al.  (R,S)-Ketamine Metabolites (R,S)-norketamine and (2S,6S)-hydroxynorketamine Increase the Mammalian Target of Rapamycin Function , 2014, Anesthesiology.

[21]  Dennis S. Charney,et al.  Rapid and Longer-Term Antidepressant Effects of Repeated Ketamine Infusions in Treatment-Resistant Major Depression , 2013, Biological Psychiatry.

[22]  Christos G. Gkogkas,et al.  Autism-related deficits via dysregulated eIF4E-dependent translational control , 2012, Nature.

[23]  M. Austin,et al.  The mTOR signaling pathway in the prefrontal cortex is compromised in major depressive disorder , 2011, Progress in Neuro-Psychopharmacology and Biological Psychiatry.

[24]  E. Kavalali,et al.  NMDA Receptor Blockade at Rest Triggers Rapid Behavioural Antidepressant Responses , 2011, Nature.

[25]  Nanxin Li,et al.  mTOR-Dependent Synapse Formation Underlies the Rapid Antidepressant Effects of NMDA Antagonists , 2010, Science.

[26]  Christos G. Gkogkas,et al.  Postnatal deamidation of 4E-BP2 in brain enhances its association with raptor and alters kinetics of excitatory synaptic transmission. , 2010, Molecular cell.

[27]  A. Hinnebusch,et al.  Regulation of Translation Initiation in Eukaryotes: Mechanisms and Biological Targets , 2009, Cell.

[28]  D. Kupfer,et al.  Acute and Longer- Term Outcomes in Depressed Outpatients Requiring One or Several Treatment Steps: A STAR*D Report , 2006 .

[29]  Paul J Carlson,et al.  A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. , 2006, Archives of general psychiatry.

[30]  N. Sonenberg,et al.  The Translation Repressor 4E-BP2 Is Critical for eIF4F Complex Formation, Synaptic Plasticity, and Memory in the Hippocampus , 2005, The Journal of Neuroscience.

[31]  M. Meaney,et al.  The effects of chronic antidepressant treatment in an animal model of anxiety , 2004, Psychopharmacology.

[32]  K. Williams,et al.  Channel blockers acting at N-methyl-D-aspartate receptors: differential effects of mutations in the vestibule and ion channel pore. , 2002, Molecular pharmacology.

[33]  B. Spiegelman,et al.  Adipose tissue reduction in mice lacking the translational inhibitor 4E-BP1 , 2001, Nature Medicine.

[34]  John H Krystal,et al.  Antidepressant effects of ketamine in depressed patients , 2000, Biological Psychiatry.

[35]  D G Lambert,et al.  Ketamine: its mechanism(s) of action and unusual clinical uses. , 1996, British journal of anaesthesia.