It is eminently clear from numerous chapters in this volume that the orexin (hypocretin) neuropeptides are necessary for the normal expression of waking and sleep. However, it remains fundamentally unclear how the absence of signaling by these peptides results in the symptoms of narcolepsy. Which of the many neurons bearing orexin receptors are necessary to sustain normal waking and sleep, and which of the numerous orexin actions are required for these processes? Does the simple loss of orexin's excitatory actions produce narcolepsy, or are there more subtle aspects to the loss of orexin signaling that result in plastic or trophic changes that give rise to the symptoms of narcolepsy and cataplexy? (PsycINFO Database Record (c) 2016 APA, all rights reserved)
CITATION STYLE
Leonard, C. S., Kalogiannis, M., & Kohlmeier, K. A. (2011). Hypocretin/Orexin Receptor Functions in Mesopontine Systems Regulating Sleep, Arousal, and Cataplexy. In Narcolepsy (pp. 139–151). Springer New York. https://doi.org/10.1007/978-1-4419-8390-9_13
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