[BIC-announce] FW: MUHC Grand Rounds Feb. 15: Dr. R. Duman, Yale School of Medicine
Jennifer Chew, Ms.
jennifer.chew at mcgill.ca
Wed Jan 30 10:35:26 EST 2013
For your information. Jennifer
From: neuro [mailto:NEURO at LISTS.MCGILL.CA] On Behalf Of Enza Ferracane, Ms.
Sent: Friday, January 25, 2013 3:00 PM
To: NEURO at LISTS.MCGILL.CA
Subject: [NEURO] MUHC Grand Rounds Feb. 15: Dr. R. Duman, Yale School of Medicine
MUHC Psychiatry Grand Rounds RI-MUHC Mental Illness and Addiction Axis
Special Guest Speaker
Ronald Duman Ph.D.
Professor of Psychiatry and Neurobiology, Department of Psychiatry, Yale School of Medicine
Neurobiology of Stress, Depression, and Antidepressants: Remodeling Synaptic Connections
February 15th, 2013
11:00 – 12:30
South Seminar Room
P1.082
Allan Memorial Institute
1025 Pine Avenue West
Neurobiology of stress, depression, and antidepressants: remodeling synaptic connections
Molecular and cellular studies have demonstrated opposing actions of stress and antidepressants on the expression of neurotrophic factors that result in structural alterations, including regulation of neurogenesis, dendrite length and spine density in hippocampus and prefrontal cortex (PFC). The deleterious effects of stress could contribute to the reduced volume of these brain regions in depressed patients. Conversely, the actions of antidepressant treatment could be mediated in part by blocking or reversing the atrophy caused by stress and depression. Recent studies have identified a novel, rapid-acting antidepressant, ketamine that addresses the limitations of currently available agents (i.e. delayed onset of action and low response rates). We have found that ketamine, an NMDA receptor antagonist, causes a rapid induction of synaptogenesis and spine formation in the PFC via stimulation of mTOR signaling and increased synthesis of synaptic proteins. These effects of ketamine rapidly reverse the atrophy of PFC neurons caused by chronic stress and correspond to rapid behavioral responses in models of depression. Characterization of a novel signaling pathway also identifies new targets for the development of rapid and efficacious antidepressants without the side effects of ketamine.
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