PLMs index AH average of snoring h and Total sleep

PLMs index, AHÍ, average of snoring/h, and Total sleep time (TST) showed significant differences as expected by the inclusion criteria of groups (see Table 3). Cardio-respiratory variables showed a decrease percentage of oxygen saturation in the group of PLMs/severe OSAHS and OSAHS only, in relation with group of PLMs only (F=3.14; gl =5153; p=0.01), see Table 4.
Discussion
Conclusion
Introduction Major depressive disorder (MD) is a serious, recurrent, heterogeneous, and disabling psychiatric illness, that will affect one out of five people in their life-time and is the leading cause of disability worldwide; however, the current knowledge about the mechanisms associated with the pathogenesis of this disease is still limited, and current treatments remain ineffective in a large subset of patients [2,15,22]. In accordance with the monoamine theory of MD, the main order GSK1120212 of antidepressants are directed to elevate the synaptic levels of monoamines in the brain. However, these drugs are associated with several limitations, which include limited clinical efficacy, therapeutic lag with high risk of suicide and morbidity during latent period and treatment resistant cases [32,36]. Therefore, in order to improve the understanding of MD and its treatment, the study of the contribution of other neuromodulatory systems in this pathology is warranted. The hypothalamus is considered the highest hierarchical structure in the control of homeostasis, and the postero-lateral region has been considered an integrative area involved in mediating different behaviors and processes that are critical to this function. Within this and adjacent regions of the hypothalamus, there are neurons that utilize the neuropeptides melanin-concentrating hormone (MCH) or hypocretin-1 and 2 (also called orexin A and B, respectively) as neuromodulators [4,27]. Both groups of neurons project throughout the central nervous system [4,27]. Interestingly, while hypocretins have mainly an excitatory synaptic action, MCH has the opposite effect, and whereas the MCHergic system tends to conserve energy, the hypocretinergic system is considered to have catabolic survival functions [7,28]. Moreover, whereas the hypocretinergic neurons are involved in the generation and maintenance of wakefulness and degeneration of these neurons produces narcolepsy, a sleep pathology, the MCHergic system promotes sleep, mainly rapid eyes movement (REM) sleep [33,34]. The hypocretinergic system has been involved in mood regulation and reward; however, the precise role of hypocretins in behavioral and neurophysiological impairments observed in depression is still unclear. The fact that both hypoactivity and hyperactivity of the hypocretinergic system have been found to be associated with depression (see [24] for a comprehensive review), may reflect the heterogeneous nature of MD. Borowsky et al. [5] have demonstrated in rats that the MCH-R1 antagonist SNAP-7941 has an antidepressant-like profile in the forced-swim test (FST, a widely used experimental paradigm for screening antidepressant activity), suggesting that MCH is a pro-depressive neuromodulator. This finding was confirmed by preclinical studies [6,8,11,12,19,35,38], but the mechanism by which the MCHergic system participates in mood regulation is still unknown. However, recent studies showed that MCH suppresses the activity of presumed serotonergic neurons of the dorsal raphe nucleus (DRN) [9], and decreases the release of serotonin within this nucleus [37]; by this means, MCH might promote a depressive mood [19]. Recently, Schmidt et al. [30] showed that MCH serum level decreases in patients with MD during antidepressant treatment. In the present study, with the hypothesis that antidepressant pharmacological treatment decreases MCHergic activity, we analyzed the MCH concentration in the cerebro-spinal fluid (CSF) as well as the hypothalamic expression of the preproMCH (Pmch) gene in rats, following subchronical treatment with Fluoxetine (FLX), an antidepressant drug of the selective serotonin reuptake inhibitor (SSRI) group [40]. In order to know if FLX also modulates the hypocretinergic system, hypocretin-1 levels in the CSF and preprohypocretin (Hcrt) gene expression were also analyzed.