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Out for the count

Nature Reviews Neuroscience volume 2, pages 454–455 (2001)Cite this article

Previous work had shown that mice lacking the gene for orexins appear to be narcoleptic, and a single human patient has been identified in whom a mutation in this gene led to early-onset narcolepsy. In most sufferers, though, the disease is not monogenic, and the symptoms develop around adolescence. These patients show decreased orexin levels and apparent loss of the orexin-containing neurons of the lateral hypothalamic area.

In an attempt to reproduce this phenotype, Hara et al. generated mice carrying a transgene coupled to the prepro-orexin promoter so that the gene product, a truncated form of ataxin 3 with 77 polyglutamine repeats that causes apoptosis, would be expressed only in the orexin neurons. When the transgenic mice were born they appeared to be normal, but over the subsequent weeks they showed a gradual loss of orexin neurons, which was almost complete by 15 weeks.

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References

ORIGINAL RESEARCH PAPER

  1. Hara, J. et al. Genetic ablation of orexin neurons in mice results in narcolepsy, hypophagia, and obesity. Neuron 30, 345–354 (2001)

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FURTHER READING

  1. Siegel, J. M. Narcolepsy: a key role for hypocretins (orexins). Cell 98, 409–412 (1999)

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Authors
  1. Rachel Jones
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Jones, R. Out for the count. Nat Rev Neurosci 2, 454–455 (2001). https://doi.org/10.1038/35081524

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  • DOI: https://doi.org/10.1038/35081524

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