Aspects of the narcolepsy-cataplexy syndrome in O/E3-null mutant mice

A. K. De La Herrán-Arita, V. C. Zomosa-Signoret, D. A. Millán-Aldaco, M. Palomero-Rivero, M. Guerra-Crespo, R. Drucker-Colín, R. Vidaltamayo

Resultado de la investigaciónrevisión exhaustiva

18 Citas (Scopus)

Resumen

Orexins (hypocretins) are peptide neurotransmitters produced by a small group of neurons located exclusively in the lateral hypothalamus (LH). Orexins modulate arousal, and as a result, have profound effects on feeding behavior and the sleep-wake cycle. Loss of orexin producing neurons leads to a narcoleptic phenotype, characterized by sudden transitions from vigilance to rapid eye movement (REM) sleep (direct transition to REM, DREM) observed in electroencephalogram (EEG) and electromyogram (EMG) recordings. In this study, we demonstrate that mice lacking the basic helix-loop-helix transcription factor O/E3 (also known as ebf2) have a decrease in orexin-producing cells in the LH, in addition to a severely impaired orexinergic innervation of the pons. These changes in the orexinergic circuit of O/E3-null animals induce a narcoleptic phenotype, similar to the one arising in orexin-deficient and orexin-ataxin-3 mice. Taken together, our results suggest that O/E3 plays a central role during the establishment of a functional orexinergic circuit by controlling the expression of essential hypothalamic neurotransmitter and the correct development of the nerve fibers arising from the hypothalamus. This is the first report regarding the narcolepsy-cataplexy syndrome in O/E3-null mice, which adds the importance of transcription factors in the regulation of neural subpopulations that control the sleep-wake cycle.

Idioma originalEnglish
Páginas (desde-hasta)134-143
Número de páginas10
PublicaciónNeuroscience
Volumen183
DOI
EstadoPublished - 2 jun 2011
Publicado de forma externa

All Science Journal Classification (ASJC) codes

  • Neurociencia (todo)

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