• Publications
  • Influence
mTOR-Dependent Synapse Formation Underlies the Rapid Antidepressant Effects of NMDA Antagonists
TLDR
The results demonstrate that the effects of ketamine are opposite to the synaptic deficits that result from exposure to stress and could contribute to the fast antidepressant actions of ketamines. Expand
Chronic Antidepressant Treatment Increases Neurogenesis in Adult Rat Hippocampus
TLDR
Investigation of the effect of antidepressants on hippocampal neurogenesis in the adult rat using the thymidine analog bromodeoxyuridine (BrdU) as a marker for dividing cells demonstrates that chronic antidepressant treatment significantly increases the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus. Expand
A Neurotrophic Model for Stress-Related Mood Disorders
TLDR
Analysis of preclinical cellular and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies, are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation ofBDNF plays a role in the actions of antidepressant treatment. Expand
Stress, Depression, and Neuroplasticity: A Convergence of Mechanisms
TLDR
Greater appreciation of the convergence of mechanisms between stress, depression, and neuroplasticity is likely to lead to the identification of novel targets for more efficacious treatments. Expand
A molecular and cellular theory of depression.
TLDR
These findings constitute the framework for an updated molecular and cellular hypothesis of depression, which posits that stress-induced vulnerability and the therapeutic action of antidepressant treatments occur via intracellular mechanisms that decrease or increase, respectively, neurotrophic factors necessary for the survival and function of particular neurons. Expand
Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications
TLDR
Findings provide strong evidence to suggest that serum BDNF levels are abnormally low in patients suffering from major depressive disorder and that the BDNF Levels are elevated following a course of antidepressant treatment. Expand
IL-1β is an essential mediator of the antineurogenic and anhedonic effects of stress
  • J. Koo, R. Duman
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences
  • 15 January 2008
TLDR
It is demonstrated that in vivo and in vitro studies demonstrate that hippocampal neural progenitor cells express IL-1RI and that activation of this receptor decreases cell proliferation via the nuclear factor-κB signaling pathway, a critical mediator of the antineurogenic and depressive-like behavior caused by acute and chronic stress. Expand
Glutamate N-methyl-D-aspartate Receptor Antagonists Rapidly Reverse Behavioral and Synaptic Deficits Caused by Chronic Stress Exposure
TLDR
The results indicate that the structural and functional deficits resulting from long-term stress exposure, which could contribute to the pathophysiology of depression, are rapidly reversed by NMDA receptor antagonists in a mammalian target of rapamycin dependent manner. Expand
The many faces of CREB
TLDR
Emerging evidence suggests that strategies that exploit regional differences in upstream factors or that target specific CREB-regulated genes, rather than CREB itself, could make a promising contribution to the treatment of neuropsychiatric conditions. Expand
Brain-Derived Neurotrophic Factor Produces Antidepressant Effects in Behavioral Models of Depression
TLDR
The hypothesis that BDNF in the hippocampus produces an antidepressant effect in behavioral models of depression, the learned helplessness (LH) and forced swim test (FST) paradigms is tested and provides further support for the hypothesis thatBDNF contributes to the therapeutic action of antidepressant treatment. Expand
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