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

J Neurosci. 2012 Feb 15;32(7):2252-62. doi: 10.1523/JNEUROSCI.5493-11.2012.


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.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Intramural

MeSH terms

  • Animals
  • Carrier Proteins / physiology*
  • Electroshock* / methods
  • Embryonic Stem Cells / physiology
  • Female
  • Hippocampus / cytology
  • Hippocampus / growth & development*
  • Hippocampus / physiology
  • Intracellular Signaling Peptides and Proteins
  • Male
  • Membrane Proteins / deficiency
  • Membrane Proteins / physiology*
  • Mice
  • Mice, 129 Strain
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Neurologic Mutants
  • Neurogenesis / physiology
  • Neuronal Plasticity / physiology*
  • Random Allocation


  • Carrier Proteins
  • Intracellular Signaling Peptides and Proteins
  • Membrane Proteins
  • tamalin protein, mouse