ライフサイエンスコーパス: VMH

1 VMH also receives moderate Ucn 3 input from the medial a

2 VMH dendrites received frequent appositions from AgRP-im

3 VMH l-NMMA injection also increased the glucose infusion

4 VMH MC3R signaling was not sufficient to rescue the lean

5 VMH Trx-1 overexpression also lowered the insulin requir

6 VMH Trx-1 overexpression normalized both the CRR and glu

7 VMH-specific inhibition of TBK-1 in mice with diet-induc

8 hh::Cre driver leads to a fate switch from a VMH neuronal phenotype to a hypothalamic but non-VMH ide

9 of the VMH and 8 days later rats received a VMH microinjection of either 1) anti-insulin affibody, 2

10 capacity of the ephrinA5 ligand to activate VMH EphA5 receptors, and if so, whether these changes co

11 e Sprague-Dawley rats that received an acute VMH microinjection of ephrinA5-Fc, chronic VMH knockdown

12 Furthermore, altering VMH glucosensing by raising or lowering glucokinase (GK)

13 Thus, although VMH glucosensing does not appear to be involved in eithe

14 Whether the PMd, AHN and VMH are involved in unconditioned fear to another predat

15 ontrast, electrolytic lesions of the AHN and VMH reduced freezing to TMT while not affecting conditio

16 gest that fibers passing through the AHN and VMH, and not cells in the MHDC, mediate unconditioned fr

17 sity of ERbeta positive cells in the AMY and VMH than males.

18 l, changes in gene expression in the ARC and VMH appeared to be largely due to changes in area rather

19 ene plays a key role in establishing ARC and VMH nuclei in mice.

20 on increased Deptor mRNA in both the ARC and VMH of obese rats.

21 st, we show that Rax is expressed in ARC and VMH progenitors throughout development, consistent with

22 ed STAT-3 protein phosphorylation in Arc and VMH.

23 After insulin, blood and VMH glucose reached nadirs by 30-40 min, and the same ra

24 , meal patterns were observed, and blood and VMH microdialysis fluid were sampled in 15 rats every 10

25 Intracerebroventricular and VMH injection of the nonselective NOS inhibitor N(G)-mon

26 ver, VMH beta-hydroxybutyrate (beta-OHB) and VMH-to-serum beta-OHB ratio levels were higher in HFD ra

27 the POA was larger in males, and the POA and VMH of breeding animals were larger than those of non-br

28 t (HFD; 60%) intake on feeding and serum and VMH FA levels, rats were trained to eat a low-fat diet (

29 tudy illustrates that Rax is required in ARC/VMH progenitors to specify neuronal phenotypes within th

30 he broader elimination of Rax throughout ARC/VMH progenitors using Six3::Cre leads to a severe loss o

31 uated in Sprague-Dawley rats after bilateral VMH injections of 1) a GK activator drug (compound A) to

32 Finally, re-expression of PREP by bilateral VMH injection of adeno-associated virus-PREP reversed th

33 ved, via implanted guide cannulae, bilateral VMH microinjections of 1) artificial extracellular fluid

34 tocin (STZ)-diabetic rats received bilateral VMH microinjections of an adenoassociated viral vector c

35 otypes, demonstrating a role for Rax in both VMH and ARC fate specification.

36 trate that CD36 is a critical factor in both VMH neuronal FA sensing and the regulation of energy and

37 ing Six3::Cre leads to a severe loss of both VMH and ARC cellular phenotypes, demonstrating a role fo

38 ed glucagon increase was attenuated (40%) by VMH insulin microinjection.

39 sistent with the behavior changes induced by VMH to AHN pathway activation, direct activation of the

40 rmalized both the CRR and glucose sensing by VMH GI neurons in STZ rats.

41 r, NAC does not normalize glucose sensing by VMH GI neurons when RH occurs during diabetes.

42 e VMH microinjection of ephrinA5-Fc, chronic VMH knockdown, or overexpression of ephrinA5 using an ad

43 In conclusion, VMH BDNF reduces body weight by decreasing food intake a

44 RAMPs1-3, CTR1a,b) are expressed in cultured VMH astrocytes, neurons, and microglia, as well as in mi

45 ses nitric oxide (NO) production in cultured VMH glucose-inhibited neurons.

46 n fact, using calcium imaging in dissociated VMH neurons showed that ketone bodies overrode normal FA

47 fibers are found in the POA, SCN, PVN, DMH, VMH, and ARC.

48 lamic areas, notably the POA, SCN, PVN, DMH, VMH, supraoptic nucleus, and the ventral and dorsal prem

49 deletion in PVH neurons projecting to either VMH or LPBN results in hyperphagia and obesity.

50 We postulated that amylin enhances VMH leptin signaling by inducing interleukin (IL)-6, whi

51 Therefore, although the entire VMH including the VMH(vl) shares a common lineage, the V

52 At birth, extensive VMH projections to broad regions of the brain were obser

53 Finally, VMH glucose-inhibited neurons were virtually absent in n

54 , suggesting that Rax is a selector gene for VMH cellular fates.

55 ether, our data reveal a neural circuit from VMH to PVT that inhibits food intake.

56 a led us to hypothesize that NO release from VMH glucose-inhibited neurons is critical for the CRR.

57 Furthermore, VMH-specific SF-1 KO mice showed significantly decreased

58 To understand how VMH neurons exercise output functions and describe an an

59 However, VMH beta-hydroxybutyrate (beta-OHB) and VMH-to-serum bet

60 However, VMH CD36-depleted rats did have increased plasma leptin

61 gh articles, on the Virtual Metabolic Human (VMH) database which links human and gut microbiota metab

62 Moreover, during hypoglycemia, VMH GABA levels did not change in the diabetic animals,

63 pothalamic (AHN), ventromedial hypothalamic (VMH) and dorsal premammillary nuclei (PMd), has been pro

64 The response of ventromedial hypothalamic (VMH) glucose-inhibited neurons to decreased glucose is i

65 ns, or into the ventral medial hypothalamus (VMH), which contains predominantly VGLUT2-containing glu

66 he ventromedial nucleus of the hypothalamus (VMH) at the same dose that disrupted female selective re

67 he ventromedial nucleus of the hypothalamus (VMH) influences a wide variety of physiological response

68 ventral medial nucleus of the hypothalamus (VMH) is a key site of FOXO1 action.

69 he ventromedial nucleus of the hypothalamus (VMH) plays a critical role in regulating systemic glucos

70 he ventromedial nucleus of the hypothalamus (VMH) was higher during breeding and non-breeding compare

71 he ventromedial nucleus of the hypothalamus (VMH), as demonstrated by behavioral pharmacology experim

72 ssess the role of ventromedial hypothalamus (VMH) (arcuate plus ventromedial nucleus) glucosensing ne

73 ng neurons in the ventromedial hypothalamus (VMH) alter their activity when ambient levels of metabol

74 egions, including ventromedial hypothalamus (VMH) and lateral parabrachial nucleus (LPBN).

75 The ventromedial hypothalamus (VMH) and the brain melanocortin system both play vital r

76 The ventromedial hypothalamus (VMH) and the central melanocortin system both play vital

77 ng neurons in the ventromedial hypothalamus (VMH) are active and required during this behavior.

78 arcuate (Arc) and ventromedial hypothalamus (VMH) as well as the area postrema (APOS) and nucleus of

79 ronal FA sensing, ventromedial hypothalamus (VMH) CD36 was depleted using adeno-associated viral (AAV

80 due to changes in ventromedial hypothalamus (VMH) exposure to insulin, bilateral guide cannulas were

81 between islet and ventromedial hypothalamus (VMH) glucose sensing, we tested the hypothesis that the

82 red activation of ventromedial hypothalamus (VMH) glucose-inhibited (GI) neurons by low glucose after

83 ansmission in the ventromedial hypothalamus (VMH) in response to hypoglycemia and to elucidate the ef

84 ctions within the ventromedial hypothalamus (VMH) influence counterregulatory hormone responses durin

85 ansmission in the ventromedial hypothalamus (VMH) is crucial for full activation of counterregulatory

86 depletion in the ventromedial hypothalamus (VMH) of mice resulted in hyperphagic behavior and obesit

87 rojections to the ventromedial hypothalamus (VMH) or lateral periaqueductal gray (lPAG) drives escape

88 g) neurons in the ventromedial hypothalamus (VMH) play an important role in regulating body weight, F

89 rter SGLT1 in the ventromedial hypothalamus (VMH) plays a role in glucose sensing and in regulating t

90 The ventromedial hypothalamus (VMH) plays chief roles regulating energy and glucose hom

91 l recognized that ventromedial hypothalamus (VMH) serves as a satiety center in the brain.

92 ng neurons in the ventromedial hypothalamus (VMH) that are critical for male territorial aggression.

93 The ventromedial hypothalamus (VMH) was thought to be essential for coping with threat,

94 The ventromedial hypothalamus (VMH), a critical node in the neural networks regulating

95 released into the ventromedial hypothalamus (VMH), a key brain glucose-sensing region in the response

96 n the BDNF mutant ventromedial hypothalamus (VMH), an energy balance-regulating center.

97 itory tone in the ventromedial hypothalamus (VMH), an important glucose-sensing region in the brain,

98 of neurons in the ventromedial hypothalamus (VMH), especially those residing in the dorsomedial part

99 In the rat ventromedial hypothalamus (VMH), leptin-induced action potential firing was enhance

100 in the brain, the ventromedial hypothalamus (VMH), plays an important role in modulating the magnitud

101 possibly via the ventromedial hypothalamus (VMH), to increase leptin signaling and phosphorylation o

102 s mediated by the ventromedial hypothalamus (VMH), which contains specialized glucosensing neurons, m

103 on located in the ventromedial hypothalamus (VMH).

104 ygdala (AMY), and ventromedial hypothalamus (VMH).

105 n the MAN and the ventromedial hypothalamus (VMH).

106 and resting metabolic rate (RMR); and 3) if VMH BDNF thermogenic effects are mediated by uncoupling

107 , our results indicate that PI3K activity in VMH neurons plays a physiologically relevant role in med

108 with genetic inhibition of PI3K activity in VMH neurons showed a sexual dimorphic obese phenotype, w

109 Changes in VMH AKT activation of diet-induced obese Lin28aKI(VMH) o

110 croinjection techniques to assess changes in VMH GABA levels and the effects of GABA(A) receptor bloc

111 We found that mGluR5 depletion in VMH SF1 neurons did not affect energy balance regulation

112 lycemic meals were preceded by 5 min dips in VMH (but not blood) glucose levels, neither blood nor VM

113 cess controlled by mitochondrial dynamics in VMH regulation of systemic glucose homeostasis.

114 for 5 days increased IL-6 mRNA expression in VMH explants and microglia by two- to threefold, respect

115 5% of all spontaneous meals, with no fall in VMH levels.

116 anscriptional networks modulated by FOXO1 in VMH neurons are key components in the regulation of ener

117 65) protein as well as a twofold increase in VMH GABA levels compared with controls under baseline co

118 wed enhanced leptin and insulin signaling in VMH neurons from mice lacking PTP1B in SF-1 neurons.

119 ssion and reduced reactive oxygen species in VMH neurons mediated by dynamin-related peptide 1 (DRP1)

120 a GK activator drug (compound A) to increase VMH GK activity, 2) low-dose alloxan (4 mug) to acutely

121 These data suggest that increased VMH GABAergic inhibition is an important contributor to

122 ory failure in RH and diabetes by increasing VMH GABA levels.

123 These results show that amylin-induced VMH microglial IL-6 production is the likely mechanism b

124 aloric intake as a consequence of FA-induced VMH ketone body production by astrocytes.

125 factor 1 (SF1) rapidly inhibits food intake, VMH SF1 neurons project dense fibers to the paraventricu

126 We 1) measured changes in interstitial VMH glutamate levels by using microdialysis and biosenso

127 Intra-VMH melanocortin receptor activation also induced signif

128 Intra-VMH MTII enhanced activity-related EE even when activity

129 Lastly, intra-VMH MTII induced mRNA expression of muscle energetic med

130 We show that intra-VMH melanocortin receptor activation increases energy ex

131 We also show that intra-VMH melanocortin receptor activation increases sympathet

132 red to vehicle-treated rats, rats with intra-VMH melanocortin receptor activation had higher skeletal

133 Conversely, Lin28aKD(VMH) mice displayed glucose intolerance and insulin resi

134 s (Lin28aKI(VMH) ) or downregulate (Lin28aKD(VMH) ) Lin28a expression in mice.

135 diet-induced obese Lin28aKI(VMH) or Lin28aKD(VMH) mice were not associated with alterations in Let-7

136 re not affected in Lin28aKI(VMH) or Lin28aKD(VMH) mice.

137 se homeostasis were not affected in Lin28aKI(VMH) or Lin28aKD(VMH) mice.

138 KT activation of diet-induced obese Lin28aKI(VMH) or Lin28aKD(VMH) mice were not associated with alte

139 ight and composition were observed, Lin28aKI(VMH) mice showed improved glucose tolerance and insulin

140 s (VMH) to selectively overexpress (Lin28aKI(VMH) ) or downregulate (Lin28aKD(VMH) ) Lin28a expressio

141 Conversely, local VMH blockade of insulin amplified glucagon twofold to th

142 ving higher serum levels, HFD rats had lower VMH FA levels but ate less from 3 to 6 h of refeeding th

143 4CIN or OX lowered VMH GABA levels in both RH and diabetic rats and restore

144 Whole-cell recordings in BDNF mutant VMH neurons revealed normal calcium currents but reduced

145 mediated alpha2delta-1 rescue in BDNF mutant VMH significantly mitigates their hyperphagia, obesity,

146 However, like NAC, VMH Trx-1 overexpression did not prevent HAAF or normali

147 neuronal phenotype to a hypothalamic but non-VMH identity, suggesting that Rax is a selector gene for

148 not blood) glucose levels, neither blood nor VMH levels declined before second meals, suggesting that

149 ucleus, the ventromedial hypothalamic nuclei(VMH)and the lateral hypothalamus are sensitive to a numb

150 in the ventral medial hypothalamic nucleus (VMH) and is required for the development of this nucleus

151 ) and the ventromedial hypothalamic nucleus (VMH) mediating control of male and female sexual behavio

152 ct in the ventromedial hypothalamic nucleus (VMH) to regulate body weight homeostasis.

153 ssed in neurons of the ventromedial nucleus (VMH) and colocalized with proopiomelanocortin (POMC) in

154 al of 370 hypothalamic ventromedial nucleus (VMH) glutamatergic neurons was studied using whole-cell

155 The hypothalamic ventromedial nucleus (VMH) is important in regulating energy metabolism.

156 geted the hypothalamic ventromedial nucleus (VMH) to selectively overexpress (Lin28aKI(VMH) ) or down

157 ed in the hypothalamic ventromedial nucleus (VMH), and the activation of AMPK in this area is suffici

158 rvate the hypothalamic ventromedial nucleus (VMH), and Ucn 3 injection into the VMH suppresses feedin

159 ucleus (PVN) or in the ventromedial nucleus (VMH), restored plasma glucose.

160 antly expressed in the ventromedial nucleus (VMH), where it regulates glucose-induced neuronal activa

161 ns of the hypothalamic ventromedial nucleus (VMH).

162 However, chronic depletion by 26-70% of VMH GK mRNA reduced glucoprivic feeding.

163 Activation of VMH EphA5 receptors via targeted microinjection of ephri

164 not prevent HAAF or normalize activation of VMH GI neurons by low glucose in STZ rats after RH.

165 o hypoglycemia in vivo and the activation of VMH GI neurons in low glucose using membrane potential s

166 assays to show that selective activation of VMH neurons expressing steroidogenic factor 1 (SF1) rapi

167 The dendritic arbor of VMH neurons was somewhat different in the vlVMH vs. the

168 However, the anatomical basis of VMH-mediated SNS activation has thus far proved elusive.

169 Neither blockade of VMH B1AR nor B3AR suppressed counterregulatory responses

170 anipulations and chemical-genetic control of VMH neuronal circuitry, we unmasked that this mitochondr

171 ches in mice, we describe the development of VMH efferent projections, as marked by steroidogenic fac

172 otocol was also used to assess the effect of VMH delivery of a selective B1AR or B3AR antagonist.

173 -alpha (ERalpha) stimulates neural firing of VMH neurons expressing ERalpha, and these effects are bl

174 have been born, suggesting that formation of VMH circuitry begins at the onset of neurogenesis.

175 Importantly, bilateral inhibition of VMH ketone production with a 3-hydroxy-3-methylglutaryl-

176 In addition, inhibition of VMH PI3K activity blocked effects of 17beta-estradiol to

177 erexpression increased, whereas knockdown of VMH ephrinA5 reduced counterregulatory responses during

178 Both models of VMH-specific SF-1 KO were susceptible to high fat diet-i

179 d, and a comparison with the organization of VMH afferents in lizards suggests a homologous similarit

180 Overexpression of VMH ephrinA5 transiently increased local glutamate conce

181 Local stimulation of VMH EphA5 receptors by ephrinA5-Fc or ephrinA5 overexpre

182 e conditional ablation of Rax in a subset of VMH progenitors using a Shh::Cre driver leads to a fate

183 5 knockdown produced profound suppression of VMH interstitial fluid glutamine concentrations in the b

184 llowing its binding to the Htr2c receptor on VMH neurons, serotonin uses a calmodulin kinase (CaMK)-d

185 However, 2-DG infusion to the MAN or VMH under normoglycemic conditions had no systemic effec

186 st via reverse microdialysis into the PVN or VMH attenuated the effect of systemic E2 on plasma gluco

187 moderate CB1 signals, including the LA, Pa, VMH, LM, and PMV, were dominated by glutamatergic neuron

188 and metabolism involves divergent pathways; VMH MC3R signaling improves metabolic homeostasis but do

189 n the brain, we generated pre- and postnatal VMH-specific SF-1 KO mice.

190 , and regulated by estrogen signaling in PR+ VMH neurons.

191 We show that projections of PR+ VMH neurons to the anteroventral periventricular (AVPV)

192 L-lactate raised VMH GABA levels and suppressed counterregulatory respons

193 blish whether lactate contributes to raising VMH GABA levels in these two conditions.

194 The shRNA reduced VMH SGLT1 expression by 53% in nondiabetic rats, and thi

195 ct downstream of BDNF to critically regulate VMH neuronal activity and metabolic function.

196 Although restoring VMH MC3R signaling also had a modest impact on obesity,

197 The paucity of rPFH-VMH Ucn 3 projection is consistent with the finding that

198 Despite significant VMH CD36 depletion, there was no effect on food intake,

199 omote glucose counterregulation via specific VMH beta-adrenergic receptors (BAR).

200 Strikingly, VMH projections were visible early, at embryonic (E) 10.

201 e, suggesting that AgRP may influence target VMH neurons.

202 To target VMH MC3R expression, we used the steroidogenic factor-1

203 We conclude that VMH NO production is necessary for glucose sensing in gl

204 mmary, our genetic tracing studies show that VMH efferent projections are highly conserved in rodents

205 Because of recent evidence showing that VMH activation modulates skeletal muscle metabolism, we

206 These studies suggest that VMH GK activity is an important regulator of the counter

207 the first 1 h of refeeding, suggesting that VMH astrocyte ketone production mediated their reduced i

208 The VMH is innervated by UCN3 neurons that arise mainly from

209 E2 administration in both the PVN and the VMH resulted in peripheral insulin resistance.

210 propose the existence of an axis between the VMH and skeletal muscle, modulated by brain melanocortin

211 e that express Cre in neurons expressing the VMH-specific transcription factor steroidogenic factor 1

212 However, the feeding circuit for the VMH regulation of food intake remains to be defined.

213 or PTP1B in regulating insulin action in the VMH and suggest that increased insulin responsiveness in

214 f the pool of glucose-excited neurons in the VMH and that this process regulates systemic glucose hom

215 emia, and if so, whether knockdown of in the VMH can improve counterregulatory responses to hypoglyce

216 istent with the role of melanocortins in the VMH in the modulation of skeletal muscle metabolism.

217 rt the role of melanocortin receptors in the VMH in the modulation of skeletal muscle metabolism.

218 e study were to determine: 1) if BDNF in the VMH increases energy expenditure (EE); 2) if BDNF-enhanc

219 criptional programs regulated by SF-1 in the VMH is not well defined.

220 glutamate receptor subtype 5 (mGluR5) in the VMH is regulated by caloric status in normal mice and re

221 rved an increase in methyl HIS levels in the VMH of AMN, LEP and AMN+LEP-treated rats.

222 e, glutamic acid decarboxylase (GAD), in the VMH of control and recurrently hypoglycemic rats.

223 ally, in contrast to deletion of Bdnf in the VMH of mice, which resulted in increased intake of stand

224 Activation of melanocortin receptors in the VMH of rats using a non-specific agonist melanotan II (M

225 pressed Trx-1 (cytosolic form of Trx) in the VMH of rats with streptozotocin (STZ)-induced type 1 dia

226 red [4-(13)C]glutamine concentrations in the VMH of RH animals.

227 to measure extracellular GABA levels in the VMH of two diabetic rat models, the diabetic BB rat and

228 ly avian-specific neuronal activation in the VMH of zebra finch parents.

229 denervation blunted the effect of E2 in the VMH on both EGP and hepatic insulin sensitivity.

230 These findings suggest that SGLT1 in the VMH plays a significant role in the detection and activa

231 Our previous work indicated that BDNF in the VMH reduced food intake.

232 during the clamp, activation of B2AR in the VMH significantly lowered by 32% (P < 0.01), whereas VMH

233 te acts through kainic acid receptors in the VMH to augment counterregulatory responses.

234 thesis that melanocortin peptides act in the VMH to increase EE by lowering the economy of activity v

235 nd glutamine/glutamate concentrations in the VMH were assessed during a hyperinsulinemic-hypoglycemic

236 Next, weanling rats were injected in the VMH with CD36 AAV shRNA.

237 eover, our results imply that neurons in the VMH(vl) adopt a distinct fate early in development, whic

238 ied glutamate metabolic enzyme levels in the VMH, 4) examined astrocytic glutamate reuptake mechanism

239 Furthermore, E2 administration in the VMH, but not in the PVN, increased EGP and induced hepat

240 ecreased LepR expression specifically in the VMH, leading to leptin resistance.

241 Thus, in the VMH, leptin negatively regulates FI, promoting weight lo

242 ly in VGLUT1-containing neurons, and, in the VMH, pVGLUT1lac showed an approximately 10-fold preferen

243 10-fold more cells in POR cortex than in the VMH, whereas a control vector supported expression in si

244 increased whereas c-Fos was decreased in the VMH.

245 a direct FOXO1 transcriptional target in the VMH.

246 (A) receptors or knockdown of GAD(65) in the VMH.

247 educed astrocytic glutamate transport in the VMH.

248 efore, although the entire VMH including the VMH(vl) shares a common lineage, the VMH(vl) further dif

249 ere found in other brain areas including the VMH.

250 al extracellular fluid or L-lactate into the VMH and sample for GABA.

251 Local catecholamine release into the VMH enhances counterregulatory responses to hypoglycemia

252 origin of the Ucn 3 afferent input into the VMH is unknown.

253 BDNF (0.5 microg) was injected into the VMH of male Sprague-Dawley rats and oxygen consumption,

254 nd diabetes, we injected 4CIN or OX into the VMH of RH and diabetic rats before inducing hypoglycemia

255 mines that the major Ucn 3 afferent into the VMH originates from the PVHap/pBNST.

256 actate dehydrogenase, oxamate (OX), into the VMH prior to inducing hypoglycemia.

257 nucleus (VMH), and Ucn 3 injection into the VMH suppresses feeding.

258 ing the VMH(vl) shares a common lineage, the VMH(vl) further differentiates into a neuronal cluster d

259 in the dorsomedial and central parts of the VMH (VMHdm/c), and observed a range of context-dependent

260 ent evidence suggests that activation of the VMH alters skeletal muscle metabolism.

261 e cannulas were inserted to the level of the VMH and 8 days later rats received a VMH microinjection

262 steroidogenic factor 1 (SF-1) neurons of the VMH are lean due to increased energy expenditure.

263 anatomical evidence to support a role of the VMH in respiratory regulation.

264 of the AHN nor ibotenic acid lesions of the VMH reduced freezing in shock-induced conditioned or TMT

265 ease is in part mediated at the level of the VMH under both normoglycemic and hypoglycemic conditions

266 o increased SPA and RMR, suggesting that the VMH is an important site of BDNF action to influence ene

267 biologically meaningful stimuli and that the VMH may be influenced by dopamine to alter female respon

268 Thus, the present study indicates that the VMH may modulate sympathetic and autonomic activity via

269 ding compared with molt, suggesting that the VMH may play a role in the estrogen-dependent regulation

270 % when the B2AR agonist was delivered to the VMH (P < 0.01) and suppressed by 32% with the B2AR antag

271 Hap/pBNST) of the population projects to the VMH and the caudal part (rPFH) co-localizes with Enk and

272 elements in the fiber complex lateral to the VMH by using immunoelectron microscopy.

273 els that was prevented by coinjection to the VMH of a GABA(A) receptor agonist.

274 s that the major Ucn 3 afferent input to the VMH resides in the anterior parvicellular part of the pa

275 nervation in the fiber plexus lateral to the VMH that may underlie the hormone-specific effect of OT

276 very of a GABA(A) receptor antagonist to the VMH.

277 gulatory response through actions within the VMH and the MAN.

278 sulin levels or insulin receptors within the VMH caused an immediate twofold increase in fasting gluc

279 A5/ephrinA5 system might function within the VMH during hypoglycemia to stimulate counterregulatory h

280 es in ephrinA5/EphA5 interactions within the VMH, a key brain glucose-sensing region, act in concert

281 eractions and synaptic plasticity within the VMH, a key glucose-sensing region in the brain, may cont

282 ephrinA5, but not EphA5 receptors within the VMH, was reduced by antecedent recurrent hypoglycemia.

283 These VMH efferents travel caudally through the periaqueductal

284 physiological functions associated with this VMH subregion.

285 emonstrating that Rax+ lineages give rise to VMH neurons.

286 rojecting to LPBN are distinct from those to VMH, yet Ntrk2 deletion in PVH neurons projecting to eit

287 elta-1 by gabapentin infusion into wild-type VMH significantly increases feeding and body weight gain

288 at SF1-positive neurons in the ventrolateral VMH (VMH(vl)) persist in Z/EG(Sf1:Cre) embryos but are v

289 (PVN), dorsomedial (DMH), and ventromedial (VMH) hypothalamic nuclei.

290 form) in the arcuate (ARC) and ventromedial (VMH) nuclei was increased after fasting and decreased by

291 , namely the arcuate (ARC) and ventromedial (VMH), tasked with proper signal integration.

292 or (LA), paraventricular (Pa), ventromedial (VMH), lateral mammillary (LM), and ventral premammillary

293 ion was found in the preoptic, ventromedial (VMH), paraventricular hypothalamic nuclei, and in the be

294 1-positive neurons in the ventrolateral VMH (VMH(vl)) persist in Z/EG(Sf1:Cre) embryos but are virtua

295 e nucleus of the solitary tract (NTS), where VMH efferents make close contacts with catecholaminergic

296 ificantly lowered by 32% (P < 0.01), whereas VMH B2AR blockade raised by 27% exogenous glucose requir

297 ses to hypoglycemia and investigated whether VMH GABAergic tone is altered in diabetes and therefore

298 productive behavior, but the degree to which VMH is involved in female reproductive behavior is uncle

299 ism by which amylin treatment interacts with VMH leptin signaling to increase its effect on weight lo

300 or an HFD in 3 h/day and were monitored with VMH FA microdialysis.