ライフサイエンスコーパス: MCH

1 MCH also modulates sleep, drug abuse behavior, and mood,

2 MCH cells are thought to be GABAergic, releasing GABA to

3 MCH cells promote memory and appropriate stimulus-reward

4 MCH has no effect on kisspeptin-insensitive GnRH, vGluT2

5 MCH immunoreactive fibers are in close proximity to vGlu

6 MCH in late gestation promotes molecular maturation of t

7 MCH increased expression of genes regulating hypoxia sig

8 MCH increased expression of genes regulating sodium (SCN

9 MCH increased fetal lung expression of the anti-oxidant

10 MCH is implicated in a number of behaviors but direct ev

11 MCH is produced by a distinct population of neurons loca

12 MCH promoted surfactant maturation (SFTP-B, SFTP-D, ABCA

13 MCH receptor (MCHR1) activation in the AcbSh increases f

14 th melanin concentrating hormone receptor 1 (MCH-R1) in the LHA, and genetic disruption of kappaOR re

15 Melanin-concentrating hormone receptor 1 (MCH-R1) is a G-protein-coupled receptor (GPCR) and a tar

16 the coinage metal dimethylmetallates, [CH(3)MCH(3)](-) (M = Cu, Ag and Au), were examined under the

17 In addition, MCH suppressed action potential firing MSNs through K(+)

18 g an essential player, whereas in adipocytes MCH induces metabolic pathways that promote lipid storag

19 d the inhibition of a centrally administered MCH-evoked drinking effect, and compound 5m exhibited or

20 In adults, MCH neurons maintain a hyperpolarized membrane potential

21 Although MCH is expressed in the gastrointestinal tract, its role

22 c enhancement of the ISR does not ameliorate MCH or SAH-induced DWMI.

23 d virtually were tested experimentally in an MCH-R1 competitive binding assay, and six novel chemotyp

24 iving Hcrt (P = 0.18, t = 1.39, df = 14) and MCH (P = 0.28, t = 1.39, df = 14) cells relative to cont

25 led little interaction between TRH axons and MCH neurons, but showed TRH axons terminating on or near

26 Hcrt and MCH cells were lost throughout the anterior to posterior

27 s that we found between the loss of Hcrt and MCH neurons and the clinical stage of PD, in contrast to

28 The losses of Hcrt and MCH neurons are significantly correlated with the clinic

29 es sleep, drug abuse behavior, and mood, and MCH receptor antagonists are currently being developed a

30 l innervations between hypocretin/orexin and MCH neurons.

31 ling, regulates the expression of orexin and MCH.

32 urochemically distinct from LHA hcrt/orx and MCH cells, but partly resemble hcrt/orx cells in their g

33 AuNPs, such that the AuNPs lost shelter and MCH increased the attraction force between AuNPs.

34 Unlike TH and MCH axons, Hcrt axons are scattered throughout the regio

35 wise, mice receiving treatments with an anti-MCH antibody, either prophylactically or after the estab

36 As MCH outcomes continue to improve nationally, ethnic mino

37 is study presents a circuit analysis between MCH and LS neurons and confirms their functional connect

38 ry measure to assess the association between MCH indicators and ethnicity.

39 analysis of an association observed between MCH and the alpha-globin gene cluster variants demonstra

40 Both MCH and MCHR1 are expressed in mouse and human islets an

41 ty of hybridization signal exhibited by both MCH and ORX mRNA-expressing neurons peaked in distinct i

42 Some of the neurons affected by MCH were likely serotonergic on the basis of their elect

43 hich neuropeptide receptors are expressed by MCH neurons by using double in situ hybridization.

44 d to determine whether they are expressed by MCH neurons.

45 e of these other signaling molecules made by MCH neurons remains incompletely characterized.

46 austrum contains a significant projection by MCH axons, whereas it is devoid of TH projections.

47 Our findings show that central MCH directly controls hepatic and adipocyte metabolism t

48 a minimum rate around a critical chloroform/MCH solvent ratio.

49 bases for population-based studies comparing MCH indicators between ethnic minorities between Jan 1,

50 alamus (LH), areas of the brain that contain MCH- and orexin- synthesizing neurons in the central ner

51 rabies-infected hypothalamic cells contained MCH.

52 In contrast, MCH-neuron-ablated mice showed improved glucose toleranc

53 methanone mesylate (WIN55,212,2) depolarized MCH cells and increased spike frequency; in contrast, WI

54 selective group I mGluR agonist, depolarized MCH cells and increased spike frequency.

55 GABA plays a complex role in developing MCH neurons, with its actions conditionally dependent on

56 In contrast, we found that developing MCH neurons received substantially more excitatory synap

57 Consistent with this effect, MCH attenuated hypocretin-1-induced enhancement of the f

58 es not appear to play a major role in either MCH or SAH-induced DWMI and is therefore not a likely ta

59 f the ISR has no detectable effect on either MCH or SAH-induced DWMI.

60 demonstrate that PSPMNs synthesizing either MCH or orexin are present within LH, where they form two

61 se monocytic cells, which express endogenous MCH receptor, we found that treatment with MCH enhanced

62 es feeding and decreases energy expenditure; MCH knockout mice are lean and have a higher metabolism

63 termined whether co-infected neurons express MCH or orexin.

64 cerebral peduncle are more likely to express MCH.

65 riggering puberty and maintaining fertility, MCH may provide a critical link between energy balance a

66 al tissues suggests additional functions for MCH which remain largely unknown.

67 htheria toxin receptor (DTR) to the gene for MCH (Pmch).

68 s reveal a previously unappreciated role for MCH in host-bacterial interactions.

69 ide novel evidence for an autocrine role for MCH in the regulation of beta-cell mass dynamics and in

70 -time PCR analyses of islet RNA derived from MCH-KO revealed altered expression of islet-enriched gen

71 patch recordings in hypothalamic slices from MCH-green fluorescent protein transgenic mice, we found

72 colonic epithelial cells express functional MCH receptors, the activation of which induces IL-8 expr

73 whereas distinct relationships between HDC, MCH, and ORX mRNA-expressing neurons delineated specific

74 te integration of maternal and child health (MCH) and immunization services as a strategy to strength

75 We assessed maternal and child health (MCH) outcomes and service coverage among ethnic minoriti

76 matocrit (HCT), mean corpuscular hemoglobin (MCH), MCH concentration (MCHC), mean corpuscular volume

77 r volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC) a

78 thiolated aptamer and 6-mercapto-1-hexanol (MCH), whose ratio was optimized by electrochemical imped

79 lar MMP substrates and 6-mercapto-1-hexanol (MCH).

80 mental period when food consumption is high, MCH neurons are more depolarized than in the adult, and

81 d for Hcrt-1, melanin concentrating hormone (MCH) and alpha synuclein and glial fibrillary acidic pro

82 ns containing melanin concentrating hormone (MCH) and GABA send long axons throughout the brain and p

83 urons, namely melanin-concentrating hormone (MCH) and hypocretin/orexin (hcrt/orx), were not detected

84 Melanin-concentrating hormone (MCH) and hypocretin/orexin neurons in the lateral hypoth

85 nic hormones, melanin-concentrating hormone (MCH) and orexin, were significantly elevated in response

86 ese INRs with melanin concentrating hormone (MCH) and tyrosine hydroxylase immunoreactive neurons of

87 that utilize melanin-concentrating hormone (MCH) as a neuromodulator are localized in the postero-la

88 Orexin and melanin-concentrating hormone (MCH) have been implicated in mediating a variety of diff

89 that express melanin-concentrating hormone (MCH) in adult Lep(ob/ob) mice had no effect on food inta

90 Melanin-concentrating hormone (MCH) is a 19-amino-acid cyclic neuropeptide that acts in

91 Melanin concentrating hormone (MCH) is a cyclic neuropeptide present in the hypothalamu

92 Melanin concentrating hormone (MCH) is a hypothalamic neuropeptide known to play a crit

93 Melanin-concentrating hormone (MCH) is a hypothalamic neuropeptide that acts via MCH re

94 Melanin-concentrating hormone (MCH) is expressed primarily in the hypothalamus and has

95 Melanin-concentrating hormone (MCH) is implicated in the feeding behavior in mammals af

96 Melanin-concentrating hormone (MCH) is involved in the regulation of feeding, water bal

97 Melanin-concentrating hormone (MCH) is produced mainly in the LH, and its receptor (MCH

98 activation of melanin-concentrating hormone (MCH) neurons during intake of the artificial sweetener s

99 on identified melanin-concentrating hormone (MCH) neurons was studied using patch-clamp recording in

100 ctive loss of melanin concentrating hormone (MCH) neurons were generated.

101 in/orexin and melanin-concentrating hormone (MCH) neurons.

102 not adjacent melanin-concentrating hormone (MCH) neurons; suggesting that wake-active orexinergic ne

103 at synthesize melanin-concentrating hormone (MCH) or hypocretin/orexin.

104 Melanin-concentrating hormone (MCH) regulates feeding and complex behaviors in mammals

105 Melanin-concentrating hormone (MCH) regulates vital physiological functions, including

106 hypothalamic melanin-concentrating hormone (MCH) system that promotes feeding and decreases energy e

107 Melanin-concentrating hormone (MCH) was initially identified in mammals as a hypothalam

108 percentage of melanin-concentrating hormone (MCH)+/Fos+ neurons in the PF-LHA did not change after mu

109 exin (OX) and melanin concentrating hormone (MCH), 3) special induction of NPY expression in the dors

110 receptor for melanin-concentrating hormone (MCH), a lateral hypothalamic peptide critical for feedin

111 oxylase (TH), melanin-concentrating hormone (MCH), and hypocretin (Hcrt) in the region of the claustr

112 europeptides, melanin-concentrating hormone (MCH), and orexin (Orx).

113 xylase (HDC), melanin-concentrating hormone (MCH), and orexin/hypocretins (ORX) produced in the hypot

114 ed orexin and melanin-concentrating hormone (MCH), but male rats had a predominance of MCH directed t

115 tin/orexin or melanin concentrating hormone (MCH), have been shown to participate in sleep regulation

116 n/hypocretin, melanin-concentrating hormone (MCH), thyrotropin-releasing hormone (TRH), gonadotropin-

117 tin-regulated melanin-concentrating hormone (MCH)- or orexin (OX)-expressing cells.

118 Melanin-concentrating hormone (MCH)-deficient mice are hypophagic, lean, and do not dev

119 Melanin-concentrating hormone (MCH)-expressing neurons have been ascribed many roles ba

120 Melanin-concentrating hormone (MCH)-producing neurons are known to regulate a wide vari

121 neuropeptide melanin concentrating hormone (MCH).

122 pocretins) or melanin concentrating hormone (MCH).

123 of orexin and melanin-concentrating hormone (MCH).

124 LH melanin-concentrating-hormone (MCH) and orexin/hypocretin (OH) neurons mediate energy a

125 H), or sleep (melanin-concentrating hormone; MCH).

126 an diameter [MD], 20 mm; median clock-hours [MCH], 6) were treated with topical IFNalpha2b (n = 12),

127 en investigated, but less is known about how MCH neurons are regulated.

128 However, MCH cell dynamics during wakefulness are unknown, leavin

129 However, MCH neurons express other neurotransmitters, including G

130 also saw a substantial loss of hypothalamic MCH neurons.

131 ated the effect of maternal chronic hypoxia (MCH) for a month in late gestation on fetal lung develop

132 ll-established in vivo mild chronic hypoxia (MCH) mouse model and a new severe acute hypoxia (SAH) mo

133 inoid agonists and antagonists on identified MCH or hypocretin neurons in green fluorescent protein-e

134 To chemically identify MCH-targeted cell populations that play a role in energy

135 en together, these results clearly implicate MCH in inflammatory processes in the intestine and perha

136 Importantly, MCH blocks the excitatory effect of kisspeptin on vGluT2

137 In MCH cells, depolarizing WIN55,212,2 actions were abolish

138 We then expressed channel rhodopsin-2 in MCH neurons and photostimulated MCH projections to deter

139 ent in wild-type controls, was attenuated in MCH-KO.

140 the frequency of fast GABAergic currents in MCH cells, an effect blocked by antagonists of OH but no

141 ced electrically evoked synaptic currents in MCH cells.

142 to wild type, mice genetically deficient in MCH had substantially reduced local inflammatory respons

143 roup I mGluRs increased spontaneous EPSCs in MCH neurons, possibly by stimulation of nearby mGluR-exp

144 enterica serovar Typhimurium) was induced in MCH-deficient mice and their wild-type littermates.

145 r observation of increased beta-cell mass in MCH-overexpressing mice.

146 specifically express the reporter ZsGreen in MCH neurons show that histamine strongly inhibits MCH ne

147 roposed to excite their neighbors, including MCH neurons, suggesting that LH may sometimes coengage i

148 Together, group I mGluRs increase MCH neuron activity by multiple presynaptic and postsyna

149 ion of MCH and adenoviral vectors increasing MCH signaling were performed in rats and mice.

150 latelet count (PLT), red blood cell indices (MCH and MCV) and HDL cholesterol.

151 ed in vivo inhibition of a centrally induced MCH-induced drinking effect and exhibited a dose-depende

152 and bed nucleus of stria terminalis inhibit MCH cells.

153 onist, montrelin, dose-dependently inhibited MCH neurons.

154 ts indicate that histamine directly inhibits MCH neurons through H3R by activating GIRK channels and

155 eurons show that histamine strongly inhibits MCH neurons, an effect which is TTX insensitive, and blo

156 Together, our data suggest that TRH inhibits MCH neurons by increasing synaptic inhibition from local

157 Also, injecting MCH potentiates cocaine-induced hyperactivity in mice.

158 alamus local inhibitory cells that innervate MCH neurons.

159 blished reports of interventions integrating MCH and immunization service delivery were reviewed by s

160 Interestingly, MCH enhanced insulin secretion in human and mouse islets

161 First, we determined that rhodamine-labeled MCH (R-MCH), when microinjected into the lateral ventric

162 Mice lacking MCH (MCH-KO) on either a C57Bl/6 or 129Sv genetic backgr

163 e have previously reported that mice lacking MCH develop attenuated intestinal inflammation when expo

164 positive energy balance; thus, mice lacking MCH or MCHR1 are lean, hyperactive, and resistant to die

165 Three weeks later MCH neurons were stimulated for 1 min every 5 min for 24

166 In the liver, MCH triggers lipid accumulation and lipid uptake, with c

167 The relationship between fish and mammalian MCH systems is not well understood.

168 uctural and functional ortholog of mammalian MCH and help elucidate the nature of MCH evolution among

169 igh peptide sequence homology with mammalian MCH.

170 Mice lacking MCH (MCH-KO) on either a C57Bl/6 or 129Sv genetic background

171 it (HCT), mean corpuscular hemoglobin (MCH), MCH concentration (MCHC), mean corpuscular volume (MCV),

172 ), RBC count, mean corpuscular volume (MCV), MCH and MCHC] and the G6PD locus on Xq28 [lead SNP rs105

173 treated the electrode with mercaptohexanol (MCH) to ensure that the remaining unoccupied surfaces of

174 lene) (OPV) assemblies in methylcyclohexane (MCH) upon addition of chloroform as a good solvent is sh

175 complete immunotherapy in 7 eyes (MD, 12 mm; MCH, 9) over a median period of 5 months and immunoreduc

176 immunoreduction by 74% in 5 eyes (MD, 20 mm; MCH, 3), allowing for subsequent surgical excision (n =

177 ompletely resolved larger tumors (MD, 30 mm; MCH, 6) over a 6-month period.

178 ng inhibited action potential firing in most MCH neurons, an effect that required GABAA but not dynor

179 understand the synaptic mechanisms of mouse MCH neurons, we performed neuroanatomical mapping and ch

180 , sPLA(2)-IIA, lipocalin 2, IGFBP3, multiple MCH class II proteins, and the Na-Pi cotransporter type

181 eurons send numerous projections to multiple MCH receptor-rich targets with presumed roles in sensory

182 lox) genotype) results in increased neuronal MCH and orexin expression and increased food consumption

183 halamus, neurotensin, but neither orexin nor MCH neurons, expressed tdTomato.

184 where they directly synapse with OX, but not MCH, neurons.

185 The ability of MCH to reduce cell firing in the AcbSh is consistent wit

186 Conversely, animals with ablation of MCH neurons no longer prefer sucrose to sucralose and sh

187 For these phenotypes, ablation of MCH neurons recapitulated knock-out of MCH, so MCH appea

188 In the absence of MCH, infected mice had increased mortality associated wi

189 s (LS) contained the densest accumulation of MCH nerve terminals.

190 eir importance for the orexigenic actions of MCH.

191 Genetic activation of MCH receptors or infusion of MCH specifically in the lat

192 We showed that the activation of MCH receptors promotes nonalcoholic fatty liver disease

193 ces that shows TRH modulates the activity of MCH neurons.

194 Chronic central administration of MCH and adenoviral vectors increasing MCH signaling were

195 the DRN; the juxtacellular administration of MCH reduced the discharge in 80% of these neurons.

196 eir ability to reveal the molecular basis of MCH regulation.

197 n, and identify direct neural controllers of MCH neurons.

198 The structure-based development of MCH-R1 and other GPCR antagonists is hampered by the lac

199 However, the wide distribution of MCH receptors in peripheral tissues suggests additional

200 we demonstrate a strong inhibitory effect of MCH on an exclusive population of septal vGluT2-GnRH neu

201 There was no effect of MCH on fetal plasma/lung tissue cortisol concentrations,

202 The inhibitory effects of MCH are reproducible and nondesensitizing and are mediat

203 s of MCH, the direct postsynaptic effects of MCH have never been reported in CNS neurons.

204 we investigated potential direct effects of MCH on monocyte/macrophage functions critical for defens

205 Finally, TRH attenuated the excitation of MCH neurons by hypocretin.

206 we detected increased colonic expression of MCH and its receptor in patients with inflammatory bowel

207 exclusion of Foxa2 and reduced expression of MCH and orexin.

208 Despite the clinical implications of MCH, the direct postsynaptic effects of MCH have never b

209 c activation of MCH receptors or infusion of MCH specifically in the lateral hypothalamic area modula

210 Inhibition of MCH neurons may contribute to the TRH-mediated reduction

211 TRH inhibition of MCH neurons was attenuated by Na(+)-Ca(2+) exchanger (NC

212 The TRH inhibition of MCH neurons was eliminated by bicuculline and tetrodotox

213 bitor, abolishes histaminergic inhibition of MCH neurons.

214 grams and reviewed reports of integration of MCH services with immunization programs at the service d

215 Similarly, the percentage loss of MCH cells was lowest in stage I (12%) and was highest in

216 Similarly, there was an increased loss of MCH cells with disease severity.

217 Here biochemical and cellular mechanisms of MCH action in the rodent AcbSh are described.

218 , we demonstrated that the microinjection of MCH into the lateral ventricle results in a significant

219 sly, we demonstrated that microinjections of MCH into the DRN resulted in an increase in REM sleep an

220 -applied OH peptides occurs in a minority of MCH cells.

221 ening in vivo) with electrical monitoring of MCH cells in mouse brain slices.

222 mmalian MCH and help elucidate the nature of MCH evolution among vertebrates.

223 on of MCH neurons recapitulated knock-out of MCH, so MCH appears to be the critical neuromodulator re

224 e previously reported that overexpression of MCH is associated with mild obesity.

225 Photostimulation of MCH projections evoked a monosynaptic glutamate release

226 e (MCH), but male rats had a predominance of MCH directed to iWAT.

227 To further characterize the role of MCH in host defense mechanisms against intestinal pathog

228 Consistent with a potential role of MCH in intestinal pathology, we detected increased colon

229 Considering the role of MCH in regulating energy balance and of GnRH and kisspep

230 this study, we further explored the role of MCH in the endocrine pancreas.

231 Herein, we sought to investigate the role of MCH, an orexigenic neuropeptide specifically expressed i

232 To determine the roles of MCH neurons in vivo, we targeted expression of the human

233 been ascribed many roles based on studies of MCH-deficient mice.

234 Identifying the cellular targets of MCH is an important step to understanding the mechanisms

235 claustrum in cognitive functions and that of MCH in REM sleep.

236 w that cannabinoids have opposite effects on MCH and hypocretin neurons.

237 fects of most classical neurotransmitters on MCH neurons have been studied, but those of most neurope

238 , were immunopositive for either orexin-A or MCH.

239 HA hypocretin/orexin neurons, but not CRH or MCH neurons, in the LHA.

240 come from hypocretin/orexin, but not CRH or MCH, neurons in the LHA.

241 increased CRH, but not hypocretin/orexin or MCH gene expression, as dehydration-anorexia develops.

242 a implicate CRH but not hypocretin/orexin or MCH neurons in the LHA in the motor events associated wi

243 re substantially mediated through orexins or MCH.

244 ation of a population of LH neurons, in part MCH containing, is necessary for PS to occur.

245 other technologies (e.g., BIO-PCR, IMS-PCR, MCH-PCR).

246 odopsin-2 in MCH neurons and photostimulated MCH projections to determine their effect on LS activity

247 we determined that rhodamine-labeled MCH (R-MCH), when microinjected into the lateral ventricle, is

248 ingly, several receptors thought to regulate MCH neurons displayed minimal colocalization with MCH, s

249 and its corresponding MCH1 peptide resemble MCH found in other fish, the zebrafish Pmch2 gene and MC

250 wild-type mice with intact MCHR1 signaling, MCH significantly attenuated the hypocretin-1-induced en

251 gic neurons may be responsible for silencing MCH neurons during wakefulness and thus may be directly

252 H neurons recapitulated knock-out of MCH, so MCH appears to be the critical neuromodulator released b

253 rance through signaling molecules other than MCH.

254 h dopamine receptors (D1R and D2R), and that MCH increases spike firing when both D1R and D2R are act

255 We conclude that MCH neurons regulate glucose tolerance through signaling

256 We conclude that MCH reduces the activity of serotonergic neurons of the

257 Finally, in vivo recordings confirmed that MCH reduces neuronal cell firing in the AcbSh in freely

258 ining neurons to examine the hypothesis that MCH modulates hypocretin/orexin-mediated effects on beha

259 ion between these two systems, implying that MCH may exert a unique inhibitory influence on hypocreti

260 Our findings indicate that MCH neurons are not exclusively GABAergic and reveal a g

261 he arousal neurons are active indicates that MCH stimulation can powerfully counteract the combined w

262 provide evidence in both rats and mice that MCH neurons express histamine-3 receptors (H3R), but not

263 Recent studies have revealed that MCH neurons receive projections from several wake-promot

264 ns in awake freely moving mice, we show that MCH neurons generate conditional population bursts.

265 We further show that MCH neurons project to reward areas and are required for

266 in islet secretory function and suggest that MCH is part of a hypothalamic-islet (pancreatic) axis.

267 These results also suggest that MCH neurons may not be under MnPN inhibitory control.

268 The MCH effect was dose dependent, pertussis toxin sensitive

269 erpendicular to pi(MX)) is influenced by the MCH angle because it determines the orientation of the a

270 cal responses and behaviors regulated by the MCH system have been investigated, but less is known abo

271 these enhanced inflammatory responses in the MCH knockout mice were associated with disproportionally

272 pi*(CC) in ethylene; thus, delta11 is in the MCH plane and is perpendicular to the MC internuclear di

273 l, channelrhodopsin-2, was inserted into the MCH neurons of wild-type mice.

274 Furthermore, administration of the MCH receptor-1 antagonist GSK-856464 [4-(4-ethyl-5-methy

275 nels and suggest that that inhibition of the MCH system by wake-active histaminergic neurons may be r

276 , we further show that acute blockade of the MCH system not only reduces cocaine self-administration,

277 insight into how neuropeptides regulate the MCH system, we investigated which neuropeptide receptors

278 ting that they may not directly regulate the MCH system.

279 To selectively stimulate the MCH neurons the gene for the light-sensitive cation chan

280 Thus, the MCH system has an important modulatory role in cocaine r

281 rs, six have never before been linked to the MCH system.

282 ic neuropeptide that acts in rodents via the MCH receptor 1 (MCHR1) to regulate a wide variety of phy

283 d on either a suspected interaction with the MCH system or demonstrated high expression levels in the

284 erozygous Pmch(DTR/+) mice lost 98% of their MCH neurons.

285 This MCH cell activity correlates with novelty exploration, i

286 During fasting, Foxa2 binds to MCH and orexin promoters and stimulates their expression

287 in brain-wide maps of monosynaptic inputs to MCH and OH cells, and demonstrate optogenetically that V

288 a role in hypothalamic signaling relating to MCH neuron modulation of food intake and energy metaboli

289 a calcium indicator genetically targeted to MCH neurons showed that excitation by bath-applied OH pe

290 Here, we identify and characterize two MCH genes in zebrafish, Pmch1 and Pmch2.

291 p to understanding the mechanisms underlying MCH actions.

292 In this study, we used MCH receptor-1 knock-out (MCHR1 KO) and wild-type (WT) m

293 ypothesized that hypothalamic PSPMNs utilize MCH or orexin as their neurotransmitter.

294 is a hypothalamic neuropeptide that acts via MCH receptor 1 (MCHR1) in the mouse.

295 and infertility of Lep(ob/ob) mice, whereas MCH-expressing neurons have only a minor role.

296 d to exhibit significant colocalization with MCH neurons: nociceptin/orphanin FQ opioid receptor (NOP

297 eurons displayed minimal colocalization with MCH, suggesting that they may not directly regulate the

298 mproved glucose tolerance when compared with MCH-deficient mutant mice and wild-type mice.

299 AMPAR-mediated synaptic events (mEPSCs) with MCH treatment.

300 s MCH receptor, we found that treatment with MCH enhanced the phagocytic capacity of these cells.