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 Basal VMH GABA concentrations were more than threefold higher

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 echanism of AgRP actions on these excitatory VMH cells appears to be independent of the actions of me

51 Massive numbers of GFP-expressing VMH dendrites extended out of the core of the nucleus in

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

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

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

58 It is essentially unknown how VMH circuits underlying these innate responses develop,

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

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

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

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

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

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

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

66 he ventromedial nucleus of the hypothalamus (VMH) in these mice, compared with control animals whose

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 he ventromedial nucleus of the hypothalamus (VMH), with its major subdivisions, the dorsomedial and v

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 POA, AMY, and the ventromedial hypothalamus (VMH), a region typically involved in female reproductive

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

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

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

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

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

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

99 on located in the ventromedial hypothalamus (VMH).

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

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

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

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

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

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

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

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

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

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

110 5% of all spontaneous meals, with no fall in VMH levels.

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

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

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

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

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

116 Compound A increased VMH GK activity sixfold in vitro and reduced the epineph

117 in GABA levels, and glybenclamide increased VMH GABA levels by 57%.

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

119 current study, we examined whether increased VMH GABAergic tone may contribute to suppression of coun

120 Since conditions associated with increased VMH GK expression are associated with a blunted counterr

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

122 se, we tested the hypothesis that increasing VMH GK activity would similarly attenuate, while decreas

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

126 Intra-VMH melanocortin receptor activation also induced signif

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 4CIN or OX lowered VMH GABA levels in both RH and diabetic rats and restore

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 ns of the hypothalamic ventromedial nucleus (VMH).

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

162 Activation of VMH EphA5 receptors via targeted microinjection of ephri

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

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

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

166 progesterone treatment on dendritic arbor of VMH neurons.

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

168 Neither blockade of VMH B1AR nor B3AR suppressed counterregulatory responses

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

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

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

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

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

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

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

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

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

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

179 Overexpression of VMH ephrinA5 transiently increased local glutamate conce

180 other hand, acute and chronic reductions of VMH GK mRNA or activity had a lesser and more selective

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 L-lactate raised VMH GABA levels and suppressed counterregulatory respons

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

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

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

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

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

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

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

198 In comparison with control studies, VMH AMPK downregulation resulted in suppressed glucagon

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

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

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

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

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

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

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

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

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

208 nnate responses develop, in part because the VMH remains poorly defined at a cellular and molecular l

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

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

211 mediated selective knock-down of BDNF in the VMH and dorsomedial hypothalamus (DMH) of adult mice, we

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

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

214 a increases GABAergic inhibitory tone in the VMH and that this, in turn, suppresses glucagon and symp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

241 10-fold more cells in POR cortex than in the VMH, whereas a control vector supported expression in si

242 a direct FOXO1 transcriptional target in the VMH.

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

244 educed astrocytic glutamate transport in the VMH.

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

246 ere found in other brain areas including the VMH.

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

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

249 ypoglycemia by 40-62% when injected into the VMH in vivo.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

268 % when the B2AR agonist was delivered to the VMH (P < 0.01) and suppressed by 32% with the B2AR antag

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

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

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

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

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

274 at had been microinjected bilaterally to the VMH with an adeno-associated viral (AAV) vector expressi

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

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

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

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

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

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

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

282 nhibitory neurotransmitter, GABA, within the VMH.

283 These VMH efferents travel caudally through the periaqueductal

284 physiological functions associated with this VMH subregion.

285 Throughout, VMH GABA levels were measured using microdialysis.

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

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

288 divisions, the dorsomedial and ventrolateral VMH (dmVMH and vlVMH, respectively), has been studied ex

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

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

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

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

296 Furthermore, whereas VMH GABA levels decreased in both control and recurrentl

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.