Tamalin is a critical mediator of electroconvulsive shock-induced adult neuroplasticity.
Tamalin is a critical mediator of electroconvulsive shock-induced adult neuroplasticity.
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DOI：
10.1523/jneurosci.5493-11.2012
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发表时间：
2012-02-15
期刊：
影响因子：
--
通讯作者：
Tessarollo L
中科院分区：
文献类型：
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作者：
Yanpallewar SU;Barrick CA;Palko ME;Fulgenzi G;Tessarollo L
The molecular mechanisms underlying the effects of electroconvulsive shock therapy (ECS), a fast acting and very effective anti-depressant 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 up-regulation of the scaffold protein tamalin, selectively in the hippocampus of animals subjected to ECS. Interestingly, this gene up-regulation is functionally significant since 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.
