Characterization of the melanin‐concentrating hormone neurons activated during paradoxical sleep hypersomnia in rats

Abstract

Although the main nodes of the neuronal network that regulate paradoxical sleep (PS), also called rapid eye movement sleep, have been identified in rodents, it still needs to be more thoroughly described. We have recently shown that 58% of a hypothalamic neuronal population, the melanin-concentrating hormone (MCH) neurons, are activated after a PS hypersomnia and that MCH, when injected intracerebroventricularly, induces a dose-dependent increase in PS. This suggests that MCH plays a role in PS regulation. Two subpopulations of MCH neurons have been distinguished neurochemically, one that coexpresses cocaine and amphetamine-regulated transcript (CART) and sends ascending projections to the septum and the hippocampus, the other, the non-CART MCH neurons, send descending projections to the lower brainstem and the spinal cord. In order to better characterize the PS-activated MCH neurons it is interesting to determine whether they belong to the first, the second, or both subgroups. We therefore undertook an MCH, CART, and Fos triple immunolabeling study in PS hypersomniac rats. We showed that the MCH neurons activated during PS are part of both subpopulations since we found CART and non-CART MCH-activated neurons. Based on these results and the literature, we propose that MCH could be involved in memory processes and in the inhibition of muscle tone during PS.

Cocaine- and amphetamine-regulated transcript peptide increases spatial learning and memory in rats

“…CART was detected in the hippocampus (Abraham et al, 2005), and promoted the survival and differentiation of neurons in primary hippocampal cell culture (Wu et al, 2006). Hanriot et al (2007) suggested that melaninconcentrating hormone (MCH) cells in the hypothalamus, some of which co-contained CART, may be involved in the memory processing. Previously, it was reported that swimming in MWM generated stress, which subsides gradually during the training sessions (Aguilar-Valles et al, 2005).…”

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

“…One third of these GABAergic neurons werealso immunoreactive for the neuropeptide Melanin Concentrating Hormone (MCH). Almost 60% of all the MCH-immunoreactive neurons counted in PeF, ZI and LHA were c-Fos+ [39,46]. We recently further demonstrated that these neurons co-contain nesfatin, another recently discovered peptide [47].…”

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

“…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.…”