Melanin-concentrating hormone neurons discharge in a reciprocal manner to orexin neurons across the sleep–wake cycle

Hassani, Oum Kaltoum; Lee, Maan‐Gee; Jones, Barbara E.

doi:10.1073/pnas.0811400106

Cited by 399 publications

(375 citation statements)

References 45 publications

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“…It is in accordance with our earlier results where a similarly small amount of MCH-containing neurons was activated in control HC animals (Kitka et al 2011). In addition, the MCH-containing neurons occasionally fire during transition from wake to SWS, and they reach their maximal firing activity during REMS (Hassani et al 2009), which is probably lower than it could be during REMS rebound (Peyron et al 2009). …”

Section: Discussionsupporting

confidence: 93%

Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation

et al. 2013

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Rationale Selective rapid eye movement sleep (REMS) deprivation using the platform-on-water ("flower pot") method causes sleep rebound with increased REMS, decreased REMS latency, and activation of the melaninconcentrating hormone (MCH) expressing neurons in the hypothalamus. MCH is implicated in the pathomechanism of depression regarding its influence on mood, feeding behavior, and REMS. Objectives We investigated the effects of the most selective serotonin reuptake inhibitor escitalopram on sleep rebound following REMS deprivation and, in parallel, on the activation of MCH-containing neurons.Methods Escitalopram or vehicle (10 mg/kg, intraperitoneally) was administered to REMS-deprived (72 h) or home cage male Wistar rats. During the 3-h-long "rebound sleep", electroencephalography was recorded, followed by an MCH/Fos double immunohistochemistry. Results During REMS rebound, the time spent in REMS and the number of MCH/Fos double-labeled neurons in the lateral hypothalamus increased markedly, and REMS latency showed a significant decrease. All these effects of REMS deprivation were significantly attenuated by escitalopram treatment. Besides the REMS-suppressing effects, escitalopram caused an increase in amount of and decrease in latency of slow wave sleep during the rebound. Conclusions These results show that despite the high REMS pressure caused by REMS deprivation procedure, escitalopram has the ability to suppress REMS rebound, as well as to diminish the activation of MCH-containing neurons, in parallel. Escitalopram caused a shift from REMS to slow wave sleep during the rebound. Furthermore, these data point to the potential connection between the serotonergic system and MCH in sleep regulation, which can be relevant in depression and in other mood disorders.

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Section: Discussionsupporting

confidence: 93%

Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation

et al. 2013

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“…We recently further demonstrated that these neurons co-contain nesfatin, another recently discovered peptide [47]. In support of our Fos data, it has recently been shown in head-restrained rats that MCH neurons fire exclusively during PS [48]. Importantly, MCH neurons start to fire simultaneously with the onset of PS and therefore can play a role in PS maintenance but not in PS induction.…”

Section: Role Of the Posterior Hypothalamus In Particular Mch Neuronsupporting

confidence: 87%

Paradoxical (REM) sleep genesis by the brainstem is under hypothalamic control

Luppi

Olivier

Fort

2013

Current Opinion in Neurobiology

100

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“…The VLPO sends inhibitory projections to many arousal-promoting nuclei, including the LC and TMN (Sherin et al, 1996). Cells in the lateral hypothalamus that express melanin-concentrating hormone are also active during sleep (Modirrousta et al, 2005;Hassani et al, 2009) and project to arousal-promoting nuclei (Saito et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Sleep Homeostasis Modulates Hypocretin-Mediated Sleep-to-Wake Transitions

Carter¹,

Adamantidis²,

Ohtsu³

et al. 2009

J. Neurosci.

223

160

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The hypocretins (Hcrts) (also called orexins) are two neuropeptides expressed in the lateral hypothalamus that play a crucial role in the stability of wakefulness. Previously, our laboratory demonstrated that in vivo photostimulation of Hcrt neurons genetically targeted with ChR2, a light-activated cation channel, was sufficient to increase the probability of an awakening event during both slow-wave sleep and rapid eye movement sleep. In the current study, we ask whether Hcrt-mediated sleep-to-wake transitions are affected by light/dark period and sleep pressure. We found that stimulation of Hcrt neurons increased the probability of an awakening event throughout the entire light/dark period but that this effect was diminished with sleep pressure induced by 2 or 4 h of sleep deprivation. Interestingly, photostimulation of Hcrt neurons was still sufficient to increase activity assessed by c-Fos expression in Hcrt neurons after sleep deprivation, although this stimulation did not cause an increase in transitions to wakefulness. In addition, we found that photostimulation of Hcrt neurons increases neural activity assessed by c-Fos expression in the downstream arousal-promoting locus ceruleus and tuberomammilary nucleus but not after 2 h of sleep deprivation. Finally, stimulation of Hcrt neurons was still sufficient to increase the probability of an awakening event in histidine decarboxylase-deficient knock-out animals. Collectively, these results suggest that the Hcrt system promotes wakefulness throughout the light/dark period by activating multiple downstream targets, which themselves are inhibited with increased sleep pressure.

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Melanin-concentrating hormone neurons discharge in a reciprocal manner to orexin neurons across the sleep–wake cycle

Cited by 399 publications

References 45 publications

Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation

Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation

Paradoxical (REM) sleep genesis by the brainstem is under hypothalamic control

Sleep Homeostasis Modulates Hypocretin-Mediated Sleep-to-Wake Transitions

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