Microinjection of melanin concentrating hormone into the lateral preoptic area promotes non-REM sleep in the rat

Benedetto, Luciana; Rodriguez-Servetti, Zulma; Lagos, Patricia; D’Almeida, Vânia; Monti, Jaime M.; Torterolo, Pablo

doi:10.1016/j.peptides.2012.10.005

Cited by 47 publications

(35 citation statements)

References 33 publications

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“…Besides, animal studies showed that elevated MCH level not just antagonizes wake but has an increasing effect on SWS even if in a minor extent only (Lagos et al 2011a;Verret et al 2003). Indeed, direct injection of MCH into the ventrolateral preoptic region (VLPO) increased NREM sleep (Benedetto et al 2013). Our data show that during the sleep rebound after long-term sleep deprivation, escitalopram is still able to reduce REMS, but instead of increasing wake, it increases deep slow wave sleep.…”

Section: Discussionmentioning

confidence: 68%

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: Discussionmentioning

confidence: 68%

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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“…However, given that activation of MCH cells only doubled REM sleep in our experiments, they may have used a pharmacological dosage that exceeds the amount that is seen with the firing of MCH neurons. When Lagos and colleagues (2012) injected MCH into the basal forebrain, they reported a reduction in wake as well as an increase in REM sleep and latency to first REM bout, but when the same group injected MCH into the ventrolateral preoptic nucleus, they found that it increased NREM but not REM sleep (Benedetto et al, 2013). These studies point out the possibility that MCH may have different effects at different targets in the brain, but in our chemogenetic stimulation experiments, all of them receive MCH at the same time.…”

Section: Discussionmentioning

confidence: 99%

Melanin-concentrating hormone neurons specifically promote rapid eye movement sleep in mice

et al. 2016

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Currently available evidence indicates that neurons containing melanin-concentrating hormone (MCH) in the lateral hypothalamus are critical modulators of sleep-wakefulness, but their precise role in this function is not clear. Studies employing optogenetic stimulation of MCH neurons have yielded inconsistent results, presumably due to differences in the optogenetic stimulation protocols, which do not approximate normal patterns of cell firing. In order to resolve this discrepancy, we 1) selectively activated the MCH neurons using a chemogenetic approach (Cre-dependent hM3Dq expression) and 2) selectively destroyed MCH neurons using a genetically targeted diphtheria toxin deletion method, and studied the changes in sleep-wake in mice. Our results indicate that selective activation of MCH neurons causes specific increases in rapid eye movement (REM) sleep without altering wake or non-REM (NREM) sleep. On the other hand, selective deletions of MCH neurons altered the diurnal rhythm of wake and REM sleep without altering their total amounts. These results indicate that activation of MCH neurons primarily drives REM sleep and their presence may be necessary for normal expression of diurnal variation of REM sleep and wake.

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“…These NREMs perturbations in MCH-Vglut2KO mice could be related to the dysregulation of nocturnal REMs because MCH neurons regulate REMs by increasing the depth and adjusting the dynamics of NREMs (Varin et al 2018). In contrast, MCH neurons have also been implicated in NREMs promotion (Benedetto et al 2013; Konadhode et al 2013; Monti et al 2013; Torterolo et al 2011). …”

Section: Discussionmentioning

confidence: 99%

Melanin-concentrating hormone neurons promote rapid eye movement sleep independent of glutamate release

et al. 2018

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Neurons containing melanin-concentrating hormone (MCH) in the posterior lateral hypothalamus (LH) play an integral role in rapid eye movement sleep (REMs) regulation. As MCH neurons also contain a variety of other neuropeptides [e.g. cocaine- and amphetamine-regulated transcript (CART) and nesfatin-1] and neurotransmitters (e.g. glutamate), the specific neurotransmitter responsible for REMs regulation is not known. We hypothesized that glutamate, the primary fast-acting neurotransmitter in MCH neurons, is necessary for REMs regulation. To test this hypothesis, we deleted vesicular glutamate transporter (Vglut2; necessary for synaptic release of glutamate) specifically from MCH neurons by crossing MCH-Cre mice (expressing Cre recombinase in MCH neurons) with Vglut2flox/flox mice (expressing LoxP-modified alleles of Vglut2), and studied the amounts, architecture and diurnal variation of sleep-wake states during baseline conditions. We then activated the MCH neurons lacking glutamate neurotransmission using chemogenetic methods and tested whether these MCH neurons still promoted REMs. Our results indicate that glutamate in MCH neurons contributes to normal diurnal variability of REMs by regulating the levels of REMs during the dark period, but MCH neurons can promote REMs even in the absence of glutamate.

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Microinjection of melanin concentrating hormone into the lateral preoptic area promotes non-REM sleep in the rat

Cited by 47 publications

References 33 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

Melanin-concentrating hormone neurons specifically promote rapid eye movement sleep in mice

Melanin-concentrating hormone neurons promote rapid eye movement sleep independent of glutamate release

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