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Orexin humans

Nishino S, Ripley B, Overeem S, et al. Hypocretin (orexin) deficiency in human narcolepsy. Lancet 2000 355 39-40. [Pg.632]

Narcolepsy, a sleep disorder characterized by excessive daytime sleepiness and cataplexy, may be caused by the lack of hypocretin mRNA and peptides in humans (Peyron et al., 2000) or a disruption of the hypocretin receptor 2 or its ligand in dogs and mice (Lin et al., 1999 Chemelli et al., 1999). Hypocretin-containing neurons are located exclusively in the dorsomedial, lateral, and perifornical hypothalamic areas (Peyron et al., 1998). Two hypocretin sequences, Hcrt-1 (orexin-A) and Hcrt-2 (orexin-B), are generated from a single preprohypocretin (De Lecea et al., 1998 Peyron et al, 1998 Sakurai et al, 1998). Axons from these neurons are found in the hypothalamus, locus coeruleus (LC), raphe nuclei, tuberomamillary nucleus, midline thalamus, all levels of spinal cord, sympathetic and parasympathetic centers, and many other brain regions... [Pg.95]

Although human narcolepsy is not typically associated with orexin gene mutations, the orexin / model is most similar to the case of a narcoleptic-cataplectic child, severely symptomatic from infancy, who has a genetic defect in orexin production and release (Peyron et al., 2000). Thus, constitutive orexin deficiency alone in the presence of otherwise histologically normal orexin neurons... [Pg.412]

Figure 15.5 Exemplar EEG/EMG recordings, from an orexin/ataxin-3 rat, to show the differences between two episodes of behavioral arrest (i.e. cataplexy) (A) associated with complete muscle atonia and accompanied by an EEG with the characteristics of REM sleep, and (B) also associated with complete muscle atonia, but with minimal change to the EEG. Both of these episodes are therefore cataplectic, as characterized in the mouse and human, but only in (B) is wakefulness, and therefore consciousness, likely to be maintained. The existence of both types of episode in the rat adds support to the conceptualization of cataplexy in the human as a transitional state between wakefulness and REM sleep, or a fragmentary occurrence of REM sleep (Hishikawa Shimizu, 1995). The visual differences evident between the EEG signals recorded in these two examples were subsequently confirmed by spectral analysis. Adapted from Beuckmann et at (2004). Figure 15.5 Exemplar EEG/EMG recordings, from an orexin/ataxin-3 rat, to show the differences between two episodes of behavioral arrest (i.e. cataplexy) (A) associated with complete muscle atonia and accompanied by an EEG with the characteristics of REM sleep, and (B) also associated with complete muscle atonia, but with minimal change to the EEG. Both of these episodes are therefore cataplectic, as characterized in the mouse and human, but only in (B) is wakefulness, and therefore consciousness, likely to be maintained. The existence of both types of episode in the rat adds support to the conceptualization of cataplexy in the human as a transitional state between wakefulness and REM sleep, or a fragmentary occurrence of REM sleep (Hishikawa Shimizu, 1995). The visual differences evident between the EEG signals recorded in these two examples were subsequently confirmed by spectral analysis. Adapted from Beuckmann et at (2004).
Nishino S, Ripley B, Overeem S, Nevsimalova S, Lammers GJ, Vankova J, Okun M, Rogers W, Brooks S, Mignot E (2001) Low CSF hypocretin (orexin) and altered energy homeostasis in human narcolepsy. Ann Neurol 50 381-388... [Pg.55]

Orexins increase transmitter release. This has been shown in electrophysiolog-ical studies for acetylcholine release in the myenteric plexus of the ileum and for GABA and glutamate release in a series of locations of the central nervous system (Table 5) in other words, presynaptic orexin receptors serve as heteroreceptors. Experiments on human tissue are so far lacking. In some of the experimental models listed in Table 5 orexin-A and orexin-B were studied and orexin-B was at least as... [Pg.427]


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