Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 109, Issue 28, Pages 11378-11383Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1201191109
Keywords
despair; anhedonia; BDNF; synaptogenesis
Categories
Funding
- National Research Foundation of Korea [2011-0028317]
- Ministry of Education, Science, and Technology, Republic of Korea
- Brain Research Center of the 21st Century Frontier Research Program [2011K000264]
- US Public Health Service [MH45481, 2 P01 MH25642]
- State of Connecticut, Department of Mental Health and Addiction Services
- Natural Sciences and Engineering Research Council of Canada
- National Research Foundation of Korea [2011-0028317] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Decreased neuronal dendrite branching and plasticity of the hippocampus, a limbic structure implicated in mood disorders, is thought to contribute to the symptoms of depression. However, the mechanisms underlying this effect, as well as the actions of antidepressant treatment, remain poorly characterized. Here, we show that hippocampal expression of neuritin, an activity-dependent gene that regulates neuronal plasticity, is decreased by chronic unpredictable stress (CUS) and that antidepressant treatment reverses this effect. We also show that viral-mediated expression of neuritin in the hippocampus produces antidepressant actions and prevents the atrophy of dendrites and spines, as well as depressive and anxiety behaviors caused by CUS. Conversely, neuritin knockdown produces depressive-like behaviors, similar to CUS exposure. The ability of neuritin to increase neuroplasticity is confirmed in models of learning and memory. Our results reveal a unique action of neuritin in models of stress and depression, and demonstrate a role for neuroplasticity in antidepressant treatment response and related behaviors.
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