ライフサイエンスコーパス: POMC

1 POMC and AGRP neurons, respectively, agonize and antagon

2 POMC neurons receive orexin-A (OX-A)-expressing inputs a

3 Thus, AgRP neurons can potently affect POMC neuron function without contributing a significant

4 This novel mechanism of ER stress affecting POMC processing in DIO highlights the importance of ER s

5 Scn9a deletion in AGRP, POMC, or paraventricular hypothalamic neurons reduced EP

6 data suggest a potential role for NPY, AGRP, POMC, and CART in regulating energetic status in A. burt

7 MC neurons of the offspring prevents altered POMC projections to the preautonomic paraventricular nuc

8 sent in comparably significant numbers among POMC neurons.

9 10(-)(9)), GNPDA2 (P = 1.11 x 10(-)(8)) and POMC (P = 4.94 x 10(-)(8)) as well as a potential second

10 ually worsened glucose tolerance in AgRP and POMC IR KO mice and their respective controls but increa

11 us, including distinct responses in AgRP and POMC neuron subtypes.

12 Although AgRP and POMC neurons in the hypothalamus have long been associat

13 isualize long-range connectivity of AGRP and POMC neurons in the mouse, two molecularly defined hypot

14 uggest novel roles for antagonistic AgRP and POMC neurons in the regulation of feeding behaviors acro

15 These data reveal that AgRP and POMC neurons receive real-time information about the ava

16 tracing experiments showed that NPY/AgRP and POMC neurons were minimally affected by the knockout.

17 ell types that control food intake, AgRP and POMC neurons, in awake behaving mice.

18 vity between GABA-releasing AgRP neurons and POMC neurons was examined in brain slices from male and

19 n-specifically depolarizes both AgRP/NPY and POMC neurons but a strong inhibitory input to POMC neuro

20 sponsible for directing formation of NPY and POMC projections.

21 , urocortin, proopiomelanocortin (POMC), and POMC-derived peptides.

22 at least in part, by inhibiting anorexigenic POMC neurons remains unclear.

23 The inhibition of anorexigenic POMC neurons may be one mechanism underlying the orexige

24 decreasing the activity of the anorexigenic POMC neurons.

25 We show that, in rodents, another POMC-derived peptide, beta-endorphin, is coordinately sy

26 (ARC) in hypothalamus contains antagonizing POMC and AGRP/NPY neurons for negative and positive ener

27 ber, but not the magnitude, of activated ARC POMC neurons and is of therapeutic relevance to obesity

28 1 is an obesity suppression mechanism in ARC POMC neurons and HFD-AMPK inhibits this mechanism by pho

29 tiate the firing frequency of individual ARC POMC-EGFP cells compared with agonists alone.

30 a indicate a functional heterogeneity of ARC POMC neurons by revealing distinct subpopulations of POM

31 onto two of their postsynaptic targets (Arc POMC and paraventricular nucleus neurons), where ATP dra

32 However, unlike ARC(AgRP) neurons, ARC(POMC) neurons are extremely slow in affecting hunger (ma

33 Pro-opiomelanocortin (ARC(POMC)) neurons are viewed as the counterpoint to ARC(AgR

34 >PVH(MC4R) synapse is potentiated by the ARC(POMC) neuron-derived MC4R agonist, alpha-melanocyte stim

35 ons expressing oxytocin receptor, unlike ARC(POMC) neurons, rapidly cause satiety when chemo- or opto

36 show that hypothalamic arcuate nucleus (Arc)POMC-deficient mice, which develop severe obesity and in

37 ator of the diet-induced rewiring of arcuate POMC.

38 some endocrine cells are generated, such as POMC-positive cells in the intermediate lobe.

39 We report that OX-A/OX-1R signaling at POMC neurons promotes 2-AG biosynthesis, hyperphagia, an

40 d whether this was associated with augmented POMC neuron activation on the population and/or single-c

41 nal populations that mediate energy balance (POMC and AgRP neurons), but also into neurons critical f

42 energy balance is the proopiomelano-cortin (POMC) neuron.

43 ocessing in the majority of Nscl-2-deficient POMC neurons had no effect on energy homeostasis.

44 Brief pulses of blue light depolarized POMC-ChR2 neurons and induced the release of GABA and gl

45 gnalling is increased, resulting in enhanced POMC mRNA induction.

46 Some affected neurons express POMC; and deleting Rb1 in POMC neurons induces E2F targe

47 strate that serotonin 2C receptor-expressing POMC neurons are required to control energy and glucose

48 Approximately half of the vGlut2-expressing POMC cells also expressed Gad65.

49 In brains with low-level expression, POMC mRNA and protein was largely confined to a populati

50 In brains with high-level expression, POMC mRNA and protein was observed in the vast majority

51 First, POMC mRNA and precursor protein expression in non-neuron

52 , the anorexigenic neuropeptide alphaMSH for POMC-neurons, and two growth-stimulatory peptides, growt

53 dy fat and food intake whereas deletion from POMC neurons had no effect.

54 ether the release of GABA and glutamate from POMC terminals can be readily modulated, opioid and GABA

55 thermore, conditional Isl1 inactivation from POMC neurons impairs Pomc expression, leading to hyperph

56 neurons did not affect sIPSCs recorded from POMC neurons.

57 receptors inhibited transmitter release from POMC neurons, as did the GABA(B) receptor agonist baclof

58 Despite the reports of GABA release from POMC neurons, vGat was not detected in POMC neurons, alt

59 ely to cause a decrease in GABA release from POMC neurons.

60 functional consequence of GABA released from POMC neurons in terms of the regulation of normal energy

61 ndicates that opioids and GABA released from POMC neurons may act at presynaptic receptors on POMC te

62 ordings were made in brain slices taken from POMC-Cre transgenic mice that had been injected with a v

63 the release of amino acid transmitters from POMC neurons has not been thoroughly investigated in an

64 ugh the release of peptide transmitters from POMC neurons is regulated by energy state, whether simil

65 in addition to the peptide transmitters from POMC neurons.

66 ons dominating in lateral portions and GAD67-POMC neurons in medial portions.

67 at mRNA expression of the anorexigenic genes POMC and CART was up-regulated by 1, 2, 5 and 1, 2, resp

68 ucose and leptin signalling in glutamatergic POMC neurons is critical for determining the strength of

69 spatiotemporal pattern whereby low and high POMC syntheses in tanycytes occur periodically in each b

70 Thus, understanding how POMC neurons integrate these two signal molecules at the

71 ith epigenetic changes in fetal hypothalamic POMC and GR genes, potentially resulting in altered ener

72 Although the pathophysiology of hypothalamic POMC neurons is well understood, the genetic program tha

73 ive reporter gene expression to hypothalamic POMC neurons in transgenic mice and zebrafish.

74 d immunohistochemistry were used to identify POMC neurons and to detect the presence of mRNA for the

75 energy and glucose homeostasis and implicate POMC neurons as the target for the effect of serotonin 2

76 Abrogating insulin action in POMC neurons of the offspring prevents altered POMC proj

77 BAergic inhibitory inputs and alterations in POMC neuron activity by nutrients and adiposity signals

78 ochondria- endoplasmic reticulum contacts in POMC neurons during diet-induced obesity.

79 To the contrary, in POMC IR KO mice, insulin lowered hGP but failed to suppr

80 A (1 or 5 mum) induces an outward current in POMC neurons that is reversed by the highly selective mu

81 ve agonist DAMGO induced outward currents in POMC neurons that were completely reversed by a relative

82 at offspring showed a significant deficit in POMC neuronal functions.

83 from POMC neurons, vGat was not detected in POMC neurons, although Gad65 and Gad67 were present in ~

84 restraint stress altered Gad1 expression in POMC neurons.

85 , glutamic acid decarboxylase 67 (GAD67), in POMC neurons of both rats and mice by using in situ hybr

86 ndent deterioration of Ca(2+) homeostasis in POMC neurons during obesity development resulting in imp

87 gic recordings and GCaMP6f Ca(2+) imaging in POMC neurons in mouse brain slices indicate that maximal

88 This paradoxical increase in POMC activity was crucial for CB1R-induced feeding, beca

89 demonstrated when Htr2c loss was induced in POMC neurons in adult mice using a tamoxifen-inducible P

90 RP neurons reliably produced evoked IPSCs in POMC neurons, leading to the inhibition of POMC neuron f

91 of changes in body weight, restoring LEPR in POMC neurons normalized blood glucose and ameliorated he

92 roteins and DNA methyltransferases levels in POMC neurons.

93 The data show that somatic MORs in POMC neurons couple to multiple effectors that have diff

94 , the data show that somatodendritic MORs in POMC neurons inhibit neuronal activity through at least

95 Prolonged activation of somatic MORs in POMC neurons robustly inhibited action potential firing

96 on was used to detect vGlut2 and Gad mRNA in POMC neurons during early postnatal development.

97 ge of POMC neurons expressing vGlut2 mRNA in POMC neurons progressively decreased from approximately

98 ybridization to detect Gad1 and Gad2 mRNA in POMC neurons, as these encode the glutamate decarboxylas

99 ncreased hepatic triglyceride levels only in POMC IR KO mice, consistent with impaired lipolytic regu

100 Reexpression of LEPR only in POMC neurons in the arcuate nucleus of the hypothalamus

101 pening by the PI3K-PLC signalling pathway in POMC neurons enhances spontaneous GABA release via activ

102 sis downstream of the leptin-PI3K pathway in POMC neurons.

103 h control animals, mice lacking PPARgamma in POMC neurons had increased energy expenditure and locomo

104 Furthermore, ablation of PPARgamma in POMC neurons preserved the interaction between mitochond

105 rn stimulate mitochondrial ATP production in POMC neurons, promoting mitochondrial fusion in their ne

106 ed neurons express POMC; and deleting Rb1 in POMC neurons induces E2F target gene de-repression, cell

107 A requirement of serotonin 2C receptors in POMC neurons for the maintenance of normal energy and gl

108 tin (POMC) neurons; whether the reduction in POMC neuronal function is secondary to the microglial ac

109 ing glucose metabolism, insulin signaling in POMC neurons controls adipose tissue lipolysis and preve

110 lian target of rapamycin (mTOR) signaling in POMC neurons that elevates the ATP-sensitive potassium (

111 receptor (MOR) agonists to inhibit sIPSCs in POMC neurons when MORs were deleted from AgRP neurons, a

112 GABA-mediated spontaneous IPSCs (sIPSCs) in POMC neurons were unaffected by disturbing GABA release

113 ha secretion induces mitochondrial stress in POMC neurons that contributes to the development of obes

114 Thus, in POMC cells, the decline in the GIRK current during prolo

115 lacking the mTOR-negative regulator TSC1 in POMC neurons, but not those lacking TSC1 in NPY/AgRP neu

116 ce regulation, genetic deletion of vGlut2 in POMC neurons was accomplished using Cre-lox technology.

117 Male, but not female, mice lacking vGlut2 in POMC neurons were unable to maintain energy balance to t

118 iture accompanied by lower NPY and increased POMC mRNA levels.

119 ial fusion in their neurites, and increasing POMC neuronal firing rates and excitability.

120 ns in adult mice using a tamoxifen-inducible POMC-cre system.

121 d with channelrhodopsin AgRP neurons inhibit POMC neurons through GABA-mediated transmission.

122 These results suggest that Dyn-A inhibits POMC neurons through activation of the (kappa)2 opioid r

123 Second, unlike other known POMC-expressing cells, tanycytes rarely contained detect

124 had low-, 9 intermediate-, and 15 high-level POMC expression in tanycytes.

125 ockout mice and in mice lacking p53-mediated POMC induction in epidermal keratinocytes.

126 ation of hypothalamic pro-opio-melanocortin (POMC) neurons and impairs physiological responses to cha

127 mbined agonists activated significantly more POMC neurons (46%) compared with either drug alone ( app

128 llular activity via calcium imaging in mouse POMC-EGFP brain slices, which revealed that combined ago

129 pe and maintains a fully functional neuronal POMC phenotype throughout adulthood remains unknown.

130 Here we characterized this non-neuronal POMC expression in detail using in situ hybridization an

131 C transcripts were present, but there was no POMC protein.

132 tant role for GABAergic projections from non-POMC non-AgRP neurons to the paraventricular hypothalami

133 n of GABA release from a major subset of non-POMC, non-AgRP GABAergic neurons in the hypothalamus.

134 Furthermore, AgRP but not POMC neurons have dendritic spines and increased glutama

135 hat JNK3 deficiency in AgRP neurons, but not POMC neurons, was sufficient to cause the hyperphagic re

136 nd dose-dependently inhibits arcuate nucleus POMC neurons.

137 No effect was observed on arcuate nucleus POMC or NPY neurons.

138 7 was only expressed in approximately 10% of POMC neurons at day 1 and increased until approximately

139 ough Gad65 and Gad67 were present in ~40% of POMC neurons.

140 In mice, approximately 43% of POMC neurons contained VGLUT2, and 54% contained GAD67 m

141 y 1 and increased until approximately 45% of POMC neurons coexpressed Gad67 at 8 weeks of age.

142 In rats, approximately 58% of POMC neurons were labeled for VGLUT2 and 37% for GAD67 m

143 Approximately 7% of POMC neurons expressed vGlut2 and the highest percentage

144 ockdown of HIF-1alpha impairs the ability of POMC neurons to adapt to the changing metabolic environm

145 In contrast, absence of POMC processing in the majority of Nscl-2-deficient POMC

146 ishes, whereas DREADD-mediated activation of POMC neurons enhances CB1R-driven feeding.

147 ctivation also promotes neuronal activity of POMC cells.

148 mice is paralleled by decreased activity of POMC neurons.

149 r, biological, and functional adaptations of POMC neurons to HFD, thereby regulating whole-body energ

150 on and controls the ultimate architecture of POMC, but not AgRP, projections.

151 ty of AA phenotype is an important aspect of POMC neuron function.

152 expressed in the postsynaptic compartment of POMC neurons resist desensitization when located in the

153 thway has a pivotal role in deterioration of POMC neurons during age-dependent obesity.

154 D feeding during lactation, the formation of POMC and AgRP projections to hypothalamic target sites i

155 The impaired functioning of POMC neurons was reversed ex vivo or by parenchymal gluc

156 and elucidate the physiologic importance of POMC in tanycytes.

157 n POMC neurons, leading to the inhibition of POMC neuron firing.

158 These data suggest that direct inhibition of POMC neurons by Dyn A is mediated through the MOR, not t

159 In contrast to the strong inhibition of POMC neurons by Dyn-A, we found a weaker direct inhibito

160 signer-drugs (DREADD)-mediated inhibition of POMC neurons diminishes, whereas DREADD-mediated activat

161 lysis revealed Cadm1-positive innervation of POMC neurons via afferent projections originating from b

162 nt results show that the GABAergic nature of POMC neurons can be dynamically regulated by energy stat

163 ction significantly reduce the percentage of POMC neurons expressing Gad1 mRNA in both male and femal

164 The percentage of POMC neurons expressing vGlut2 mRNA in POMC neurons prog

165 triction, whether the GABAergic phenotype of POMC neurons is also regulated in an energy-state-depend

166 results show that the GABAergic phenotype of POMC neurons is decreased selectively by caloric deficit

167 , suggesting that the GABAergic phenotype of POMC neurons is particularly sensitive to energy deficit

168 The fact the GABAergic phenotype of POMC neurons is sensitive to energy state suggests a dyn

169 To further examine amino acid phenotypes of POMC neurons, we studied mRNA expression for the glutama

170 ic, surprisingly, only a small population of POMC neurons has been found to be glutamatergic, and a s

171 g GABAergic and glutamatergic populations of POMC neurons has been hindered by the difficulty in reli

172 structs the post-translational processing of POMC by decreasing proconverting enzyme 2, which catalyz

173 neurons, and posttranslational processing of POMC remain unaffected in response to maternal HFD feedi

174 s the excitability and neurite projection of POMC neurons, thereby causing a reduction of food intake

175 neurons, electrophysiological properties of POMC neurons, and posttranslational processing of POMC r

176 ical role of GnRH cells in the regulation of POMC neurons.

177 results reveal that GPR45 is a regulator of POMC signaling and energy expenditure, which suggests th

178 lts uncover a previously unsuspected role of POMC neurons in the promotion of feeding by cannabinoids

179 receptor would lead to a new steady state of POMC neuron activity reflecting the sustained GIRK curre

180 rons by revealing distinct subpopulations of POMC cells activated by 5-HT2CRs and disinhibited by 5-H

181 A small subset of POMC neurons appears to have a dual AA phenotype based o

182 iew and discuss the current understanding of POMC neurons from their development and intracellular re

183 ly, our findings indicate that the GLP-1R on POMC/CART-expressing ARC neurons likely mediates liraglu

184 icate a direct inhibitory effect of Dyn-A on POMC neurons through activation of the (kappa)2 opioid r

185 lts demonstrate that direct leptin action on POMC neurons does not reduce food intake, but is suffici

186 siological impact of direct leptin action on POMC neurons using a mouse model in which endogenous LEP

187 rectifying potassium (GIRK)-like channels on POMC neurons.

188 idence suggests that the action of leptin on POMC neurons regulates glucose homeostasis independently

189 actions of the antagonist at MORs located on POMC neurons.

190 OR-2-selective agonist GR89696 binds MORs on POMC neurons but fails to induce an outward current.

191 neurons may act at presynaptic receptors on POMC terminals in an autoregulatory manner to limit cont

192 contribute spontaneously released GABA onto POMC neurons, although when activated with channelrhodop

193 The presynaptic responses onto POMC neurons, and the expression of tdTomato in AgRP-NPY

194 Pro-opiomelanocortin (POMC) and agouti-related protein (AGRP) neurons in the h

195 Htr2c) specifically in pro-opiomelanocortin (POMC) neurons had normal body weight but developed gluco

196 The arcuate pro-opiomelanocortin (POMC) neurons in particular have been shown to be critic

197 ted protein (AgRP) and pro-opiomelanocortin (POMC) neurons in regulating hepatic and adipose tissue i

198 Hypothalamic pro-opiomelanocortin (POMC) neurons promote satiety.

199 nRH neurons but not in pro-opiomelanocortin (POMC) neurons reduced POMC neurons and increased viscera

200 ARC TH cells inhibited pro-opiomelanocortin (POMC) neurons through synaptic mechanisms.

201 ding satiety-promoting pro-opiomelanocortin (POMC) neurons, demonstrated opposite changes in spiking.

202 arcuate nucleus (ARC) pro-opiomelanocortin (POMC) neurons, which are also disinhibited through a 5-H

203 ection in anorexigenic pro-opiomelanocortin (POMC) neurons.

204 tone due to activated pro-opiomelanocortin (POMC) neurons.

205 er of appetite-curbing pro-opiomelanocortin (POMC) neurons; whether the reduction in POMC neuronal fu

206 AgRP) and anorexigenic pro-opiomelanocortin (POMC) neuropeptides.

207 acking ROCK1 in either pro-opiomelanocortin (POMC) or agouti-related protein neurons, mediators of le

208 c neurons that express pro-opiomelanocortin (POMC) or neuropeptide-Y (NPY) and agouti-related protein

209 ted peptide (AgRP) and pro-opiomelanocortin (POMC) subtypes, and an orexigenic somatostatin neuron po

210 Pro-opiomelanocortin (POMC)- and agouti-related peptide (AgRP)-expressing neur

211 gnaling (anorexigenic) pro-opiomelanocortin (POMC)-expressing and hunger signaling (orexigenic) agout

212 Satiety-signaling, pro-opiomelanocortin (POMC)-expressing neurons in the arcuate nucleus of the h

213 ces no net response in pro-opiomelanocortin (POMC)-expressing neurons.

214 eus (Arc), containing pro-opoiomelanocortin (POMC), neuropeptide Y (NPY) and growth hormone releasing

215 veral hypothalamic nuclei but not in AgRP or POMC neurons.

216 ng NMDA receptors (NMDARs) on either AgRP or POMC neurons.

217 Mex3c was not detected in NPY or POMC neurons but was detected in leptin-responsive neuro

218 n the arcuate nucleus, as well as onto other POMC neurons.

219 ase in genes encoding anorexigenic peptides, POMC, and somatostatin may account for the reduced body

220 y slow and long-lasting actions of peptides, POMC neurons can rapidly affect the activity of downstre

221 indicate that in addition to their peptides, POMC neurons can release either the amino acid (AA) tran

222 igh-fat diet also did not affect the portion POMC neurons expressing Gad1, suggesting that the GABAer

223 nd the highest percentage of vGlut2-positive POMC cells were located in the rostral arcuate nucleus.

224 ynaptic GABAergic terminals and postsynaptic POMC neurons.

225 ulation of hypothalamic microglia to promote POMC neuronal activation in association with hypothalami

226 elated peptide (AgRP)-, proopiomelanocortin (POMC)-, single-minded 1 (Sim1)-, or steroidogenic factor

227 rison, we also analyzed Proopiomelanocortin (POMC)-expressing neurons, an intermingled population tha

228 europeptide Y (NPY) and proopiomelanocortin (POMC) neurons in the arcuate nucleus play central roles

229 anocortin receptors and proopiomelanocortin (POMC) was analyzed by means of RT-PCR, Western immunoblo

230 egulator 1 (NEGR1), and proopiomelanocortin (POMC)] by PUFAs, only 125 genes [e.g., adiponectin, C1Q

231 ression of anorexigenic proopiomelanocortin (POMC) and orexigenic agouti-related peptide (AgRP) neuro

232 on or near anorexigenic proopiomelanocortin (POMC) cells.

233 downstream anorexigenic proopiomelanocortin (POMC)-positive neurons in a GABA-dependent manner, which

234 arcuate nucleus (ARC), proopiomelanocortin (POMC) neurons and the POMC-derived peptide alpha-melanoc

235 Arcuate proopiomelanocortin (POMC) neuron-specific deletion of Ptpn1 causes a similar

236 Neurons containing proopiomelanocortin (POMC)-derived peptides, known to control stress axis, me

237 ts in the gene encoding proopiomelanocortin (POMC) have extreme early-onset obesity, hyperphagia, hyp

238 luding those expressing proopiomelanocortin (POMC) and agouti-related peptides (AgRP).

239 d in neurons expressing proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript

240 e groups neurons [e.g., proopiomelanocortin (POMC) and agouti-related peptide (AgRP) neurons], and as

241 Hypothalamic proopiomelanocortin (POMC) is essential for the physiological regulation of e

242 Hypothalamic proopiomelanocortin (POMC) neurons and their peptide products mediate importa

243 Hypothalamic proopiomelanocortin (POMC) neurons are important regulators of energy balance

244 ization in hypothalamic proopiomelanocortin (POMC) neurons as these neurons produce the endogenous op

245 Hypothalamic proopiomelanocortin (POMC) neurons have traditionally been defined by their p

246 ctivity of hypothalamic proopiomelanocortin (POMC) neurons in mice were altered in the offspring of m

247 (MORs) in hypothalamic proopiomelanocortin (POMC) neurons leads to the activation of G-protein-coupl

248 Hypothalamic proopiomelanocortin (POMC) neurons release peptide products that potently inh

249 EY POINTS: Hypothalamic proopiomelanocortin (POMC) neurons release peptide products that potently inh

250 driver of hypothalamic proopiomelanocortin (POMC) neurons.

251 C isoform Pkc-lambda in proopiomelanocortin (POMC) neurons disrupts leptin action, reduces melanocort

252 amic neurons, including proopiomelanocortin (POMC) and agouti-related peptide (AgRP) neurons, also re

253 amic neurons, including proopiomelanocortin (POMC) and agouti-related peptide (AgRP) neurons, also re

254 intake and to increase proopiomelanocortin (POMC) gene expression in the hypothalamus.

255 KOR), directly inhibits proopiomelanocortin (POMC) neurons in the hypothalamus through activation of

256 thalamic neuron markers proopiomelanocortin (POMC), neuropeptide Y (NPY), agouti-related peptide (AGR

257 of PPARgamma in murine proopiomelanocortin (POMC) neurons decreases peroxisome density, elevates rea

258 orexigenic neuropeptide proopiomelanocortin (POMC).

259 s neuropeptide Y (NPY), proopiomelanocortin (POMC), orexin/hypocretin, melanin-concentrating hormone

260 d increased activity of proopiomelanocortin (POMC) neurons.

261 f its precursor protein proopiomelanocortin (POMC) remained unaltered.

262 eratinocytes synthesize proopiomelanocortin (POMC) that is processed to melanocyte-stimulating hormon

263 generally believed that proopiomelanocortin (POMC) is expressed exclusively by neurons in the adult r

264 rmone (CRH), urocortin, proopiomelanocortin (POMC), and POMC-derived peptides.

265 te food intake, whereas proopiomelanocortin (POMC) neurons inhibit feeding.

266 ving food intake, while proopiomelanocortin (POMC) neurons inhibit feeding.

267 H) and colocalized with proopiomelanocortin (POMC) in the arcuate nucleus (ARC).

268 ) show that hypothalamic propiomelanocortin (POMC) neurons innervate the anterior ventral V-SVZ and r

269 pro-opiomelanocortin (POMC) neurons reduced POMC neurons and increased visceral fat mass, suggesting

270 stically, we determined that GPR45 regulates POMC expression via the JAK/STAT pathway in a cell-auton

271 ion in expression of the metabolic regulator POMC and less energy expenditure prior to the onset of o

272 These neurons release POMC-encoded melanocortins, which are potent anorexigeni

273 hannel activity cell-autonomously to silence POMC neurons.

274 bd7 mRNA is expressed and translated by some POMC and GABAergic-neurons in the hypothalamic arcuate n

275 ices revealed that GLP-1 directly stimulates POMC/CART neurons and indirectly inhibits neurotransmiss

276 hibited anorexigenic neurons that synthesize POMC, as determined by whole cell recording.

277 erably more sensitive to energy deficit than POMC neurons.

278 Altogether, the results indicate that POMC neurons are largely glutamatergic early in life and

279 Recent work shows that POMC neurons can also release the amino acid transmitter

280 , proopiomelanocortin (POMC) neurons and the POMC-derived peptide alpha-melanocyte-stimulating hormon

281 well as a potential secondary signal at the POMC locus (rs2118404, P = 2.4 x 10(-)(5) after conditio

282 the brain melanocortin system, including the POMC-MC4R pathway, a mechanism also activated by leptin

283 as observed at rostral and mid levels of the POMC cell group with VGLUT2-POMC neurons dominating in l

284 inistration of melanotan-2, an analog of the POMC derivative alpha-MSH, suppressed adult obesity in G

285 the possibility that alcohol effects on the POMC system may transmit through generations.

286 esent a major functional division within the POMC cell group.

287 dings indicate that the relevance of AgRP to POMC neuron GABA connectivity depends on the state of Ag

288 e relevance of GABAergic inputs from AgRP to POMC neurons is state dependent and highlight the need t

289 OMC neurons but a strong inhibitory input to POMC neurons balances the excitation.

290 bute to the strong spontaneous GABA input to POMC neurons.

291 nificant source of spontaneous GABA input to POMC neurons.

292 ated glutamate and GABA neurotransmission to POMC neurons.

293 show that leptin's action on GABA release to POMC neurons is influenced by glucose levels.

294 ning the strength of inhibitory tone towards POMC neurons.

295 ivo, we tracked these cells using transgenic POMC-EGFP mice or by retroviral expression of GFP.

296 olated basophils from human blood, truncated POMC transcripts were present, but there was no POMC pro

297 id levels of the POMC cell group with VGLUT2-POMC neurons dominating in lateral portions and GAD67-PO

298 conditions of undernourishment, during which POMC neuronal activity is decreased.

299 energic receptors in NPY/AgRP neurons, while POMC neurons are inhibited via alpha2A - adrenergic rece

300 or failed to affect food intake of mice with POMC-specific PPARgamma ablation.