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Cortistatin overexpression in transgenic mice produces deficits in synaptic plasticity and learning

Academic Article
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Overview

authors

  • Tallent, M. K.
  • Veronique, F.
  • Qiu, C.
  • Calbet, M.
  • Lamp, T.
  • Baratta, M. V.
  • Suzuki, C.
  • Levy, C. L.
  • Siggins, George
  • Henriksen, S. J.
  • Criado, J. R.
  • Roberts, Amanda
  • de Lecea, L.

publication date

  • November 2005

journal

  • Molecular and Cellular Neuroscience  Journal

abstract

  • Cortistatin-14 (CST) is a neuropeptide expressed in cortical and hippocampal interneurons that shares 11 of 14 residues with somatostatin. In contrast to somatostatin, infusion of CST decreases locomotor activity and selectively enhances slow wave sleep. Here, we show that transgenic mice that overexpress cortistatin under the control of neuron-specific enolase promoter do not express long-term potentiation in the dentate gyrus. This blockade of dentate LTP correlates with profound impairment of hippocampal-dependent spatial learning. Exogenously applied CST to slices of wild-type mice also blocked induction of LTP in the dentate gyrus. Our findings implicate cortistatin in the modulation of synaptic plasticity and cognitive function. Thus, increases in hippocampal cortistatin expression during aging could have an impact on age-related cognitive deficits.

subject areas

  • Aging
  • Animals
  • Dentate Gyrus
  • Female
  • Gene Expression Regulation, Developmental
  • Hippocampus
  • Learning
  • Learning Disorders
  • Long-Term Potentiation
  • Male
  • Memory Disorders
  • Mice
  • Mice, Transgenic
  • Peptides
  • Promoter Regions, Genetic
  • Synaptic Transmission
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Identity

International Standard Serial Number (ISSN)

  • 1044-7431

Digital Object Identifier (DOI)

  • 10.1016/j.mcn.2005.08.010

PubMed ID

  • 16182561
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Additional Document Info

start page

  • 465

end page

  • 475

volume

  • 30

issue

  • 3

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