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Complexin II is essential for normal neurological function in mice.

Dervila Glynn1, Rachel A Bortnick, A Jennifer Morton

  • 1Department of Pharmacology, University of Cambridge, UK.

Human Molecular Genetics
|August 14, 2003
PubMed
Summary
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Complexin-II knockout mice exhibit progressive motor and cognitive deficits, particularly in reversal learning. These findings suggest Complexin-II depletion may contribute to neurological disorders like Huntington's disease.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Behavioral Genetics

Background:

  • Complexins (CPLXs) are key regulators of synaptic vesicle release.
  • Complexin-II (CPLXII) knockout (KO) mice initially appear normal but develop behavioral impairments with age.

Purpose of the Study:

  • To investigate the long-term behavioral consequences of CPLXII deficiency.
  • To explore the potential role of CPLXII depletion in neurological diseases.

Main Methods:

  • Behavioral testing in CPLXII KO mice, including rotarod, Morris water maze, two-choice swim tank, open field, and grooming assays.
  • Age-dependent assessment of behavioral deficits.
  • Comparison with Huntington's disease (HD) models.

Main Results:

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  • CPLXII KO mice show significant motor deficits (rotarod) and cognitive impairments (Morris water maze, two-choice swim tank reversal learning) that worsen with age.
  • Deficits in exploratory and social grooming behaviors are also observed.
  • These behavioral deficits are not attributable to physical weakness, indicating higher-order functional impairments.
  • The observed deficits closely mirror those in the R6/2 HD mouse model, which exhibits CPLXII depletion.

Conclusions:

  • Progressive CPLXII depletion contributes to motor and cognitive dysfunction.
  • CPLXII deficiency is implicated in the pathogenesis of Huntington's disease.
  • Reduced CPLXII expression may play a role in other diseases with combined motor, cognitive, and psychiatric symptoms, such as schizophrenia.