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Publication : Tamalin is a critical mediator of electroconvulsive shock-induced adult neuroplasticity.

First Author  Yanpallewar SU Year  2012
Journal  J Neurosci Volume  32
Issue  7 Pages  2252-62
PubMed ID  22396401 Mgi Jnum  J:181614
Mgi Id  MGI:5312150 Doi  10.1523/JNEUROSCI.5493-11.2012
Citation  Yanpallewar SU, et al. (2012) Tamalin is a critical mediator of electroconvulsive shock-induced adult neuroplasticity. J Neurosci 32(7):2252-62
abstractText  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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