Orexin and MCH neurons express c‐Fos differently after sleep deprivation vs. recovery and bear different adrenergic receptors

Modirrousta, Mandana; Mainville, Lynda; Jones, Barbara E.

doi:10.1111/j.1460-9568.2005.04104.x

Cited by 186 publications

(160 citation statements)

References 63 publications

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“…This result also differs from the findings of Modirrousta et al; they described an increase in the number of Fos immunoreactive MCHergic neurons in a paradigm of sleep rebound (mainly QS) after sleep deprivation in rats compared to wakefulness (Modirrousta, et al, 2005). However, it is interesting to note that the number of Fos expressing MCHergic neurons during the sleep rebound was small (3% of the total number of MCHergic neurons).…”

Section: Discussioncontrasting

confidence: 99%

“…MCH was stained brown while Fos, which was stained black, concentrated in the nucleus. In view of published reports of Fos labeling in MCH-containing cells of the rat during AS rebound (Verret, et al, 2003) or total sleep rebound paradigms (Modirrousta, et al, 2005), it was an unexpected finding that, in our preparation, MCHergic neurons did not exhibit Fos immunoreactivity throughout the hypothalamus in any of the conditions studied (Fig. 5).…”

Section: Fos Immunoreactivity Of Mch-containing Neuronssupporting

confidence: 50%

“…In this regard, we can not discount the fact that in our study, increasing the time the animal spent in QS, induced a small, but statistically significant increase in Fos immunoreactivity, as was found in rats. Modirrousta et al have also hypothesized that MCHcontaining and hypocretinergic neurons play opposing roles in regulating sleep, waking and energy metabolism, suggesting that MCHergic may have a role in sleep and behavioral quiescence (Modirrousta, et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

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MCH-containing neurons in the hypothalamus of the cat: Searching for a role in the control of sleep and wakefulness

Torterolo

Sampogna²,

Morales

et al. 2006

Brain Research

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Neurons that utilize melanin-concentrating hormone (MCH) and others that employ hypocretin as neurotransmitter are located in the hypothalamus and project diffusely throughout the CNS, including areas that participate in the generation and maintenance of the states of sleep and wakefulness. In the present report, immunohistochemical methods were employed to examine the distribution of MCHergic and hypocretinergic neurons. In order to test the hypothesis that the MCHergic system is capable of influencing specific behavioral states, we studied Fos immunoreactivity in MCHcontaining neurons during 1) quiet wakefulness, 2) active wakefulness with motor activity, 3) active wakefulness without motor activity, 4) quiet sleep, and, 5) active sleep induced by carbachol (AScarbachol). We determined that MCHergic neuronal somata in the cat are intermingled with hypocretinergic neurons in the dorsal and lateral hypothalamus, principally in the tuberal and tuberomammillary regions; however, hypocretinergic neurons extended more in the anteriorposterior axis than MCHergic neurons. Axosomatic and axodendritic contacts were common between these neurons. In contrast to hypocretinergic neurons, which are known to be active during motor activity and AS-carbachol, Fos immunoreactivity was not observed in MCH-containing neurons in conjunction with any of the preceding behavioral conditions. Non-MCHergic, non-hypocretinergic neurons that expressed c-fos during active wakefulness with motor activity were intermingled with MCH and hypocretin-containing neurons, suggesting that these neurons are related to some aspect of motor function. Further studies are required to elucidate the functional sequela of the interactions between MCHergic and hypocretinergic neurons and the phenotype of the other neurons that were active during motor activity.

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Section: Discussioncontrasting

confidence: 99%

Section: Fos Immunoreactivity Of Mch-containing Neuronssupporting

confidence: 50%

Section: Discussionmentioning

confidence: 99%

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MCH-containing neurons in the hypothalamus of the cat: Searching for a role in the control of sleep and wakefulness

Torterolo

Sampogna²,

Morales

et al. 2006

Brain Research

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“…Consistent with these findings, we found that OLZ induced the activation of 38% of the orexin neurons of the LH/PFA in rat brain, whereas a negligible amount of Fos-LI was seen in MCH neurons. This suggests a heterogeneity between these two groups of orexigenic neurons in regard to their neural connectivity and roles in the regulation of behavioral state (Cvetkovic et al, 2004;Modirrousta et al, 2005). Although the exact mechanism of OLZ-associated weight gain is unknown, OLZ may be better characterized by the analysis of Fos-LI in nuclei receiving projections from orexin neurons with connections to feeding-circuit regions and reward pathways of the rat brain (Harris and AstonJones, 2006).…”

Section: Discussionmentioning

confidence: 99%

Zonisamide Prevents Olanzapine-Associated Hyperphagia, Weight Gain, and Elevated Blood Glucose in Rats

Wallingford

Sinnayah

Bymaster

et al. 2008

Neuropsychopharmacol

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Olanzapine (OLZ), one of the second-generation atypical antipsychotics (SGAs), has shown relative advantages in patient adherence and outcomes. However, OLZ has also been associated with a higher incidence of weight gain than most other SGAs. Excessive weight gain may in turn contribute to long-term health concerns for some individuals. Zonisamide (ZNS), a medication approved in the United States as an adjunct in the management of epilepsy, has a diverse pharmacological profile, including sodium channel blockade, monoamine enhancement, and inhibition of carbonic anhydrase. ZNS has also been reported to cause weight loss in both humans and rodents. We hypothesized that this profile might be beneficial when co-administered with OLZ. To test this hypothesis, we evaluated the effects of OLZ on body weight, as well as the pathways known to regulate feeding behavior and arousal in the Sprague-Dawley rat. As indicated via c-Fos expression, we found an OLZ-induced activation in the nucleus accumbens and orexin neurons in the lateral hypothalamus. An OLZ-associated development of hyperphagia, weight gain and elevated blood glucose in the rat was also found. These outcomes were attenuated and reversed in the presence of concomitant ZNS. These results suggest the hypothesis that ZNS may effectively treat or prevent weight gain or metabolic changes associated with the SGAs. Future studies of this combination in patients through appropriately designed human clinical studies are encouraged.

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“…Later, a strong connection between MCH and REMS has been revealed (Kitka et al 2011;Torterolo et al 2011). Local or intracerebroventricular administration of MCH to rodents caused a marked increase in REMS; moreover, an elevated activation (increased Fos immunoreactivity) of MCH-expressing neurons has been reported during REMS rebound after a long-term sleep deprivation (Hanriot et al 2007;Kitka et al 2011;Modirrousta et al 2005;Peyron et al 2009;Torterolo et al 2011;Verret et al 2003). The increase in the time spent in REMS and the decrease in the REMS latency during the rebound following sleep deprivation are both changes similar to those described in depression.…”

Section: Introductionmentioning

confidence: 99%

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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Orexin and MCH neurons express c‐Fos differently after sleep deprivation vs. recovery and bear different adrenergic receptors

Cited by 186 publications

References 63 publications

MCH-containing neurons in the hypothalamus of the cat: Searching for a role in the control of sleep and wakefulness

MCH-containing neurons in the hypothalamus of the cat: Searching for a role in the control of sleep and wakefulness

Zonisamide Prevents Olanzapine-Associated Hyperphagia, Weight Gain, and Elevated Blood Glucose in Rats

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

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