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Tamalin Is a Critical Mediator of Electroconvulsive Shock-Induced Adult Neuroplasticity

  1. Author:
    Yanpallewar, S. U.
    Barrick, C. A.
    Palko, M. E.
    Fulgenzi, G.
    Tessarollo, L.

  2. Author Address

    [Yanpallewar, Sudhirkumar U.; Barrick, Colleen A.; Palko, Mary Ellen; Fulgenzi, Gianluca; Tessarollo, Lino] NCI, Neural Dev Sect, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.;Tessarollo, L (reprint author), NCI, Neural Dev Sect, Mouse Canc Genet Program, Ctr Canc Res, Bldg 560,Room 32-31D, Frederick, MD 21702 USA;tessarol@mail.nih.gov
    1. Year: 2012
    2. Date: Feb
  2. Journal: Journal of Neuroscience
    1. 32
    2. 7
    3. Pages: 2252-2262
  4. Type of Article: Article
  5. ISSN: 0270-6474
  1. Abstract:

    The molecular mechanisms underlying the effects of electroconvulsive shock (ECS) therapy, a fast-acting and very effective antidepressant therapy, are poorly understood. Changes related to neuroplasticity, including enhanced adult hippocampal neurogenesis and neuronal arborization, are believed to play an important role in mediating the effects of ECS. Here we show a dynamic upregulation of the scaffold protein tamalin, selectively in the hippocampus of animals subjected to ECS. Interestingly, this gene upregulation is functionally significant because tamalin deletion in mice abrogated ECS-induced neurogenesis in the adult mouse hippocampus. Furthermore, loss of tamalin blunts mossy fiber sprouting and dendritic arborization caused by ECS. These data suggest an essential role for tamalin in ECS-induced adult neuroplasticity and provide new insight into the pathways that are involved in mediating ECS effects.

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External Sources

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  2. DOI: 10.1523/jneurosci.5493-11.2012
  3. View record in Web of Science®
  4. WOS: 000300535400004

Library Notes

  1. Fiscal Year: FY2011-2012
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