Increased susceptibility to LTP generation and changes in NMDA-NR1 and -NR2B subunits mRNA expression in rat hippocampus after MCH administration

Varas, Mariana; Pérez, Mariela Fernanda; Ramírez, Oscar A.; Barioglio, Susana Rubiales de

doi:10.1016/j.peptides.2003.09.006

Cited by 41 publications

(30 citation statements)

References 56 publications

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“…We adjusted the baseline fEPSPs for all plasticity experiments to obtain the same amount of cooperativity (these experiments were done blind to the genotype). A previous study reported that in vivo MCH application lowers the induction threshold of LTP in the rat dentate gyrus (Varas et al 2003). Interestingly, this effect was delayed because it was observed 48 h after in vivo MCH injection.…”

Section: Thus the Mch-r1mentioning

confidence: 85%

Major Impairments of Glutamatergic Transmission and Long-Term Synaptic Plasticity in the Hippocampus of Mice Lacking the Melanin-Concentrating Hormone Receptor-1

Pachoud¹,

Adamantidis

Ravassard³

et al. 2010

Journal of Neurophysiology

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Pachoud B, Adamantidis A, Ravassard P, Luppi P-H, Grisar T, Lakaye B, Salin P-A. Major impairments of glutamatergic transmission and long-term synaptic plasticity in the hippocampus of mice lacking the melanin-concentrating hormone receptor-1. J Neurophysiol 104: 1417-1425, 2010. First published June 30, 2010 doi:10.1152/jn.01052.2009. The hypothalamic neuropeptide melanin-concentrating hormone (MCH) plays important roles in energy homeostasis, anxiety, and sleep regulation. Since the MCH receptor-1 (MCH-R1), the only functional receptor that mediates MCH functions in rodents, facilitates behavioral performance in hippocampus-dependent learning tasks, we investigated whether glutamatergic transmission in CA1 pyramidal cells could be modulated in mice lacking the MCH-R1 gene (MCH-R1 Ϫ/Ϫ ). We found that both ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated transmissions were diminished in the mutant mice compared with their controls. This deficit was explained, at least in part, by a postsynaptic downregulation of these receptors since the amplitude of miniature excitatory postsynaptic currents and the NMDA/AMPA ratio were decreased. Long-term synaptic potentiation (LTP) was also impaired in MCH-R1 Ϫ/Ϫ mice. This was due to an altered induction, rather than an impaired, expression because repeating the induction stimulus restored LTP to a normal magnitude. In addition, long-term synaptic depression was strongly diminished in MCH-R1 Ϫ/Ϫ mice. These results suggest that MCH exerts a facilitatory effect on CA1 glutamatergic synaptic transmission and long-term synaptic plasticity. Recently, it has been shown that MCH neurons fire exclusively during sleep and mainly during rapid eye movement sleep. Thus these findings provide a mechanism by which sleep might facilitate memory consolidation.

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Section: Thus the Mch-r1mentioning

confidence: 85%

Major Impairments of Glutamatergic Transmission and Long-Term Synaptic Plasticity in the Hippocampus of Mice Lacking the Melanin-Concentrating Hormone Receptor-1

Pachoud¹,

Adamantidis

Ravassard³

et al. 2010

Journal of Neurophysiology

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“…Interestingly, CART reduces the depolarizationinduced intracellular Ca2ϩ signal by inhibiting voltagegated Ca2ϩ channels in cultures of hippocampal neurons in a tissue-specific manner (Yermolaieva et al, 2001) and promotes survival and differentiation of cultured hippocampal neurons (Wu et al, 2006). In addition, the administration of MCH improves memory retention in cognitive tasks that strongly rely on the hippocampus (Monzon et al, 1999;Varas et al, 2002Varas et al, , 2003. Accordingly, numerous MCH-containing fibers and dense MCH receptor 1 mRNA labeling, the only functional receptor in rodents, were detected in different fields of the entire hippocampus (Saito et al, 2001).…”

mentioning

confidence: 99%

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

Hanriot

Camargo

Courau

et al. 2007

J of Comparative Neurology

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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.

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“…MCH, when injected into the hippocampus and amygdala, modulates memory retention in the one-trial step-down inhibitory avoidance test . It has also been reported that MCH injection into the hippocampus increases susceptibility to the induction of long-term potentiation in the dentate gyrus and increases expression of mRNA of the N-methyl-D-aspartate receptor subunits in the dentate gyrus [Varas et al, 2003]; these characteristics represent possible mechanisms for the memory-promoting effects of MCH. MCH neurons also project widely through the central nervous system onto neurons of the arousal system [Bittencourt et al, 1992], and may play a role in sleep-wake states.…”

Section: Mchmentioning

confidence: 95%

“…MCH is involved in a variety of physiological events including feeding and energy balance [Qu et al, 1996;Shimada et al, 1998;Ludwig et al, 2001], sexual behavior [Gonzalez et al, 1996], stress responses [Jezova et al, 1992], the neuroendocrine system [Chiocchio et al, 2001;Kennedy et al, 2001], anxiety [Gonzalez et al, 1996], seizure production [Knigge and Wagner, 1997], memory and/or learning Varas et al, 2003], and arousal regulation [Verret et al, 2003].…”

Section: Introductionmentioning

confidence: 99%

Melanin‐concentrating hormone receptor 1 antagonists for the treatment of depression and anxiety

Chaki

Yamaguchi

Yamada

et al. 2005

Drug Development Research

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Melanin-concentrating hormone (MCH) is a cyclic, 19-amino-acid neuropeptide produced in the lateral hypothalamus. MCH is implicated in a number of physiological processes including feeding behavior, energy balance, reproductive function, memory, sleep-wake regulation, and emotional states. Since the discoveries in the mid-1990 s that MCH is an appetite stimulant in rodents and that KO mice lacking MCH become lean, together with the findings that MCH receptor 1 (MCH1R) is responsible for these functions, most research has been focused on the roles of the MCH system in feeding and energy homeostasis. It is now established that MCH plays a key role in controlling feeding and energy homeostasis via MCH1R, and some pharmaceutical companies have reported nonpeptidic MCH1R antagonists with diverse structural features in the treatment of obesity. Recently, emerging lines of evidence have indicated that MCH1R plays important roles not only in feeding and energy balance but also in regulation of emotion. Indeed, MCH1R is widely distributed in the regions associated with emotion, and MCH1R antagonists have been demonstrated to exhibit antidepressant and anxiolytic effects in various rodent models. This review describes recent advances in research to clarify the involvement of MCH in depression and anxiety. The paper will also discuss the potential value of MCH1R antagonists in the treatment of depressive and anxiety disorders. Drug Dev. Res. 65:278-290, 2005.

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Increased susceptibility to LTP generation and changes in NMDA-NR1 and -NR2B subunits mRNA expression in rat hippocampus after MCH administration

Cited by 41 publications

References 56 publications

Major Impairments of Glutamatergic Transmission and Long-Term Synaptic Plasticity in the Hippocampus of Mice Lacking the Melanin-Concentrating Hormone Receptor-1

Major Impairments of Glutamatergic Transmission and Long-Term Synaptic Plasticity in the Hippocampus of Mice Lacking the Melanin-Concentrating Hormone Receptor-1

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

Melanin‐concentrating hormone receptor 1 antagonists for the treatment of depression and anxiety

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