ライフサイエンスコーパス: GnRH

1 GnRH also increased H3S28p and H3K27ac levels and also t

2 GnRH excitability is upregulated during positive feedbac

3 GnRH neuron deficiency in male mice was accompanied by i

4 GnRH neurons do not express the estrogen receptor needed

5 GnRH receptor subtypes GnRHR1 and GnRHR2 were expressed

6 GnRH regulates the pituitary gonadotropin's follicle-sti

7 GnRH secreted by cholangiocytes promotes biliary prolife

8 GnRH stimulation increases gonadotrope GLUT1 expression

9 GnRH-induced biliary proliferation was evaluated by chan

10 y drive to gonadotropin-releasing hormone 1 (GnRH) neurons, the synaptic mechanisms of which are unkn

11 ofluorescence expression patterns and RFRP-3/GnRH cross-talk are largely conserved in the NMR brain,

12 njugated to the targeting peptide [d-Lys(6)]-GnRH, generating SAN1GSC.

13 We have identified a GnRH-like neuropeptide (pQIHYKNPGWGPG-NH2) that specific

14 dministration of 18 or 36mg of leuprolide, a GnRH agonist and a larger MW peptide, via a novel ethyle

15 e observed in vivo after administration of a GnRH agonist.

16 global deletion of Kiss1r (Kiss1r(-/-)) or a GnRH neuron-specific deletion of Kiss1r (Kiss1r(d/d)) di

17 To address this, we used a GnRH peptide-modified dendrimer platform with and withou

18 n syndrome (KS) is characterized by abnormal GnRH-1ns migration, we examined whole-exome sequencing d

19 Little is known about GnRH release during sexual maturation, but it is assumed

20 that estradiol and time of day signals alter GnRH neuron responsiveness to stimuli, GFP-identified Gn

21 ported by GLUT1 expression and activity, and GnRH-induced glycolysis is recapitulated in primary gona

22 nocopied the full spectrum of nasal axon and GnRH neuron defects of SEMA3A knockout mice.

23 logy (COST) programmes - DSDnet (BM1303) and GnRH Network (BM1105) - provided the framework for groun

24 he SGK-1 promoter in the presence of Dex and GnRH, GR levels remain unchanged compared with Dex treat

25 s the success of the COST Actions DSDnet and GnRH Network and the European Reference Network for Rare

26 phosphorylation, c-Fos mRNA expression, and GnRH release.

27 ic links between craniofacial patterning and GnRH dysfunction and begin to assemble the functional ne

28 pression profile of gonadotropin subunit and GnRH receptor genes in rat pituitary in vitro and in viv

29 cally reduced H3S28p levels in untreated and GnRH-treated cells and also affected H3K27ac levels.

30 educed neurogenesis for both vomeronasal and GnRH-1ns but less severe defects in OEC development.

31 endrites, and the density of fibers apposing GnRH neurons was even greater in PNA mice (56%).

32 prostate cancer than the currently available GnRH agonists.

33 enes responded only to variations in average GnRH concentration, Fshb levels were sensitive to both a

34 actually resulted from variations in average GnRH concentration.

35 However, the link between GnRH neuron activity and their morphology remains unknow

36 arities with neuropeptides of the bilaterian GnRH, adipokinetic hormone (AKH) and corazonin family.

37 issue with the first identification of both GnRH-type and CRZ-type signalling systems in a deuterost

38 innervation of the adult median eminence by GnRH-positive neurites.

39 ted that the long-lasting effects induced by GnRH were most likely caused by rebinding since over 70%

40 dotroph secretory function during continuous GnRH treatment.

41 However, if Gli3 plays a role in controlling GnRH-1 neuronal development has not been addressed.

42 or NRP2 to position these axons for correct GnRH neuron migration, with an additional role for the N

43 RP2 and PLXNA1 have been linked to defective GnRH neuron development in mice and inherited GnRH defic

44 H-tac3a colabeled cells were observed, dense GnRH fibers surround and potentially synapse with tac3a

45 discuss the possibility that the PPE-derived GnRH neurons of Ciona resemble an ancestral cell type, a

46 monstrate that the vertebrate/deuterostomian GnRH-type and the protostomian AKH systems are orthologo

47 During embryonic development, GnRH neurons migrate along olfactory and vomeronasal axo

48 constant-release estradiol implants (OVX+E), GnRH neuron firing is suppressed in the morning (AM) by

49 Our results shed light on the long-elusive GnRH pulse generator offering new horizons for reproduct

50 relatively insensitive to loss of endogenous GnRH and continuous treatment with GnRH, probably reflec

51 in pituitary alphaT3-1 cells with endogenous GnRH receptor expression.

52 pes of the probands and resulted in enhanced GnRH neuron death during development.

53 , providing homeostatic feedback on episodic GnRH/LH release as well as positive feedback to control

54 Aergic transmission, which typically excites GnRH neurons, are independently sufficient for increasin

55 ants indicate that Ascl-1, while crucial for GnRH-1 neurogenesis, is not required for normal OEC deve

56 function of AMH as a pro-motility factor for GnRH neurons.

57 lts identify SEMA3E as an essential gene for GnRH neuron development, uncover a neurotrophic function

58 , we discovered that Ascl-1 is necessary for GnRH-1 ontogeny.

59 ent with LH pulses in the blood; a proxy for GnRH pulses.

60 release of luteinizing hormone, a proxy for GnRH, emerges abruptly as we increase the basal activity

61 induction has a preference for low-frequency GnRH pulses.

62 ctly on the pituitary cells independent from GnRH or kisspeptin and could play multiple roles in repr

63 tropin-releasing hormone (GnRH) release from GnRH neurons to control the reproductive axis.

64 ) is a potent trigger of GnRH secretion from GnRH neurons.

65 analogue of gonadotropin-releasing hormone (GnRH or LHRH), is the active pharmaceutical ingredient u

66 Gonadotropin-releasing hormone (GnRH) agonists (e.g., triptorelin) are used for androgen

67 f the use of gonadotropin-releasing hormone (GnRH) agonists to protect ovarian function have shown mi

68 ,959 were on gonadotropin-releasing hormone (GnRH) agonists, and 3,747 underwent surgical orchiectomy

69 vertebrates, gonadotropin-releasing hormone (GnRH) and gonadotropin-inhibitory hormone (GnIH), respec

70 r release of gonadotropin-releasing hormone (GnRH) and gonadotropins.

71 g release of gonadotropin releasing hormone (GnRH) and luteinizing hormone (LH) are pivotal events in

72 nonpeptide, gonadotropin-releasing hormone (GnRH) antagonist, produced partial to nearly full estrog

73 ction of the gonadotropin-releasing hormone (GnRH) axis causes a range of reproductive phenotypes res

74 ility due to gonadotropin releasing hormone (GnRH) deficiency, which is often associated with anosmia

75 eficiency in gonadotropin-releasing hormone (GnRH) have impaired sexual reproduction.

76 Gonadotropin-releasing hormone (GnRH) is a key regulator of reproductive maturation in h

77 Gonadotropin-releasing hormone (GnRH) is a trophic peptide hormone synthesized by hypoth

78 Gonadotropin-releasing hormone (GnRH) is a trophic peptide hormone that modulates reprod

79 The gonadotropin-releasing hormone (GnRH) is the master regulator of fertility and kisspepti

80 The gonadotropin-releasing hormone (GnRH) is the master regulator of fertility.

81 hypothalamic gonadotropin-releasing hormone (GnRH) leads to a marked decrease in secretion of pituita

82 e control of gonadotropin releasing hormone (GnRH) neuronal development is unknown.

83 ivity of the gonadotropin-releasing hormone (GnRH) neuronal network controlling fertility.

84 hypothalamic gonadotropin-releasing hormone (GnRH) neurons and is essential for reproductive health.

85 ck regulates gonadotropin-releasing hormone (GnRH) neurons and subsequent luteinizing hormone (LH) re

86 roperties of gonadotropin-releasing hormone (GnRH) neurons and synaptic inputs to these cells coincid

87 Gonadotropin-releasing hormone (GnRH) neurons are the final common pathway for central n

88 al output of gonadotropin-releasing hormone (GnRH) neurons controls fertility and is sculpted by sex-

89 depends upon gonadotropin-releasing hormone (GnRH) neurons generating a pulsatile pattern of gonadotr

90 Gonadotropin-releasing hormone (GnRH) neurons produce the central output controlling fer

91 Gonadotropin-releasing hormone (GnRH) neurons regulate puberty onset and sexual reproduc

92 ontrolled in gonadotropin-releasing hormone (GnRH) neurons via action potentials and neuromodulators.

93 activity of gonadotropin-releasing hormone (GnRH) neurons.

94 lity through gonadotropin-releasing hormone (GnRH) neurons.

95 dotropes and gonadotropin-releasing hormone (GnRH) neurons.

96 feedback to gonadotropin-releasing hormone (GnRH) neurons.

97 lity through gonadotropin-releasing hormone (GnRH) neurons.

98 TATEMENT The gonadotropin-releasing hormone (GnRH) pulse generator controls the pulsatile secretion o

99 pends on the gonadotropin-releasing hormone (GnRH) pulse generator, a neural construct comprised of h

100 The gonadotropin-releasing hormone (GnRH) receptor is a drug target for certain hormone-depe

101 transfer via gonadotropin-releasing hormone (GnRH) receptors (GnRHR) to extracellular signal-regulate

102 ling through gonadotropin-releasing hormone (GnRH) related receptors.

103 with reduced gonadotropin-releasing hormone (GnRH) release and infertility.

104 ch modulates gonadotropin-releasing hormone (GnRH) release from GnRH neurons to control the reproduct

105 ic pulsatile gonadotropin-releasing hormone (GnRH) release.

106 ed pulses of gonadotropin-releasing hormone (GnRH) represents a longstanding puzzle about extracellul

107 s a brake on gonadotropin-releasing hormone (GnRH) secretion during childhood.

108 mentation of gonadotropin-releasing hormone (GnRH) secretion from a few thousand hypothalamic neurons

109 egulators of gonadotropin-releasing hormone (GnRH) secretion.

110 z belongs to gonadotropin-releasing hormone (GnRH) superfamily, implying an analogous role in growth

111 ptors of the gonadotropin-releasing hormone (GnRH) superfamily.

112 eficiency of gonadotropin-releasing hormone (GnRH) that is characterized by hypogonadism with delayed

113 regulated by gonadotropin-releasing hormone (GnRH) via MAPK signaling pathways that stimulate gene tr

114 ss genes for gonadotropin-releasing hormone (GnRH), a G-protein-coupled receptor for relaxin-3 (RXFP3

115 y that binds gonadotropin-releasing hormone (GnRH), a master regulator of reproduction in vertebrates

116 by secreting gonadotropin-releasing hormone (GnRH).

117 er molecule' gonadotropin-releasing hormone (GnRH).

118 on responsiveness to stimuli, GFP-identified GnRH neurons in brain slices from OVX+E or OVX female mi

119 thing cells in the nasal mucosa, and impairs GnRH-1 neuronal migration to the brain.

120 spiroindoline system significantly improved GnRH-R antagonist potencies across several species, mand

121 hypothesized that ablation of Galphaq/11 in GnRH neurons would diminish but not completely block KP-

122 ommon inhibitory mechanism of GnIH action in GnRH neurons and gonadotropes.

123 Culturing of pituitary cells in GnRH-free conditions downregulated Fshb, Cga, and Gnrhr

124 Timely postnatal changes in GnRH expression are essential for puberty and adult fert

125 Timely postnatal changes in GnRH secretion are essential for pubertal onset.

126 ce but they displayed significant defects in GnRH-1 neuronal migration.

127 hat conveys the inhibitory action of GnIH in GnRH neurons by using the GnRH neuronal cell line, GT1-7

128 tin and vasoactive intestinal polypeptide in GnRH neuronal cell line, GT1-7.

129 ts antiangiogenic or cytotoxic properties in GnRH-R-expressing prostate and breast tumor cells.

130 evelopment, however, if Gli3 plays a role in GnRH-1 neuronal development is unclear.

131 netic restoration of kisspeptin signaling in GnRH neurons in Kiss1r(-/-) mice, functional adenogenesi

132 not directly inhibit kisspeptin signaling in GnRH neurons.

133 C6 to modulate cell movement and survival in GnRH neurons.

134 ion and that impairing microRNA synthesis in GnRH neurons leads to hypogonadotropic hypogonadism and

135 that acts both directly and through Zeb1, in GnRH neurons.

136 primates, puberty is unleashed by increased GnRH release from the hypothalamus following an interval

137 d with normal rats, accompanied by increased GnRH secretion.

138 tch with built-in feedback governs increased GnRH expression during the infantile-to-juvenile transit

139 Kisspeptin increased GnRH excitability and was essential for estradiol regula

140 Kisspeptin increased GnRH neuron response in cells from OVX and OVX+E mice in

141 are independently sufficient for increasing GnRH neuron firing rate during positive feedback or whet

142 gonadotropins reflect Galphaq/11-independent GnRH secretion and activation of the neuroendocrine-repr

143 RH secretion and that Galphaq/11-independent GnRH secretion would be sufficient to maintain fertility

144 tion values <1 bit, implying that individual GnRH-responsive cells cannot unambiguously differentiate

145 sive effects of HCD on the estradiol-induced GnRH/LH surge were overcome by neuron-specific SOCS3 kno

146 rogesterone can block the oestradiol-induced GnRH/LH surge and inhibit LH pulse frequency.

147 nRH neuron development in mice and inherited GnRH deficiency in humans.

148 llmann syndrome (KS), which causes inherited GnRH deficiency.

149 vestigated as a candidate gene for inherited GnRH deficiency.

150 entified mutations associated with inherited GnRH deficiency, but the small number of affected famili

151 roduction in birds and mammals by inhibiting GnRH and gonadotropin secretion.

152 These findings provide new insights into GnRH-1 and OECs development and demonstrate that human G

153 eedback states of the daily surge model into GnRH neurons from OVX, OVX+E AM, and OVX+E PM mice.

154 etic interrogation of families with isolated GnRH deficiency (IGD).

155 ctivation profiles of the endogenous ligand, GnRH and a well-known marketed analog, buserelin using a

156 ) transgenic mouse lines revealed that, like GnRH neurons, most hypothalamic nNOS neurons have a glut

157 m these mice, suggesting a mechanism for low GnRH/luteinizing hormone (LH) secretion.

158 s that can potentially benefit from lowering GnRH pulsatility with consequent diminished levels of pl

159 ombinant wild-type SEMA3E protected maturing GnRH neurons from cell death by triggering a plexin D1-d

160 riectomized, estradiol-treated (OVX+E) mice; GnRH neurons are suppressed in the morning and activated

161 In experiment 2, using microdialysis, GnRH and kisspeptin surges induced by E2 benzoate were s

162 c development, AMH is expressed in migratory GnRH neurons in both mouse and human fetuses and unconve

163 In silico studies of model GnRH neurons in which >1000 PSg trains were tested exhib

164 In this daily surge model, GnRH neuron intrinsic properties are shifted to favor in

165 native GnRH (1, 2, and 5) or lipid-modified GnRH (3 and 4).

166 Finally, we find that most GnRH neurons express the kisspeptin receptor GPR54 upon

167 on a polylysine core and bore either native GnRH (1, 2, and 5) or lipid-modified GnRH (3 and 4).

168 mproved stability as compared to the natural GnRH, yet they suffer from a poor pharmacokinetic profil

169 ve embryonic migration of the neuroendocrine GnRH cells to the basal forebrain, which results in redu

170 t, gonadotropin-releasing-hormone-1 neurons (GnRH-1ns) migrate from the developing vomeronasal organ

171 espiration, by the reproductive neuropeptide GnRH.

172 Although no GnRH-tac3a colabeled cells were observed, dense GnRH fib

173 eathing cells (OEC) is imperative for normal GnRH-1 neuronal migration.

174 ve and repressive signals induces the normal GnRH-fuelled run-up to correct puberty initiation, and i

175 ) stalls at this well positioned nucleosome, GnRH-induced H3S28p, possibly in association with H3K27a

176 , we show that a male-specific activation of GnRH neurons occurs 0-2 h following birth and that this

177 In vivo and in vitro administration of GnRH increased the expression of miR-200b and fibrosis m

178 usly, we demonstrated that administration of GnRH to normal rats increased intrahepatic biliary mass

179 ptor alpha (ERalpha)-expressing afferents of GnRH neurons, including kisspeptin neurons in the antero

180 ther SEMA3E or PLXND1 increased apoptosis of GnRH neurons in the developing brain, reducing innervati

181 bconnectin-3alpha, determine the capacity of GnRH neurons to be activated by kisspeptin and estradiol

182 q/11-coupled signaling as a major conduit of GnRH secretion, it also uncovers a significant role for

183 Disruption of GnRH/GnRHR signaling may be important for the management

184 ed IP1 accumulation and a longer duration of GnRH neuron firing than KP54 (115 vs. 55 minutes; P = 0.

185 The effect of GnRH administration was evaluated in normal rats and in

186 he behavioral and neurobiological effects of GnRH agonists in mice will be important to better guide

187 However, the effects of GnRH agonists on brain function and mental health are no

188 hronous activity caused robust excitation of GnRH neurons by a synaptic mechanism that also involved

189 L cholangiocytes had increased expression of GnRH compared with normal rats, accompanied by increased

190 The expression of GnRH receptors was assessed in a normal mouse cholangioc

191 cell lines and on action potential firing of GnRH neurons in brain slices.RESULTSIn healthy women, th

192 good correspondence between the frequency of GnRH release detected by FSCV in the median eminence of

193 The frequency of GnRH release in the late embryonic stage was surprisingl

194 e for AMH in the development and function of GnRH neurons and indicate that AMH signaling insufficien

195 specification, migration and/or function of GnRH neurons.

196 Homologs of GnRH and its cognate receptor have been identified in in

197 Imaging of GnRH neurons revealed greater dendritic spine density th

198 e gene 2 knockout), the hepatic knockdown of GnRH decreased IBDM and liver fibrosis.

199 In vivo and in vitro knockdown of GnRH decreased intrahepatic bile duct mass/cholangiocyte

200 for a vesicular protein in the maturation of GnRH neuronal network.

201 ans are associated with altered migration of GnRH neurons, resulting in congenital hypogonadotropic h

202 th an HR of CVD during the first 6 months of GnRH agonist therapy of 1.91 (95% CI, 1.66 to 2.20), an

203 ienced symptom remission after 2-3 months of GnRH agonist-induced ovarian suppression (leuprolide) th

204 e synaptically connected neuronal network of GnRH neurons could account for this pathology.

205 Ovarian estradiol regulates the pattern of GnRH (negative feedback) and initiates a surge of releas

206 f GDF9 shifted the characteristic pattern of GnRH pulse frequency sensitivity.

207 es in the absence and continuous presence of GnRH.

208 output, but that the intrinsic properties of GnRH neurons during positive feedback further poise thes

209 xl2 expression levels control the pruning of GnRH dendrites, highlighting an unexpected role for a ve

210 al polypeptide (VIP), positive regulators of GnRH neurons.

211 mechanism underlying the episodic release of GnRH is not known, although recent studies have suggeste

212 ently decreased the impedance as a result of GnRH receptor activation with potencies of 9.3 +/- 0.1 (

213 We evaluated the autocrine role of GnRH in the regulation of cholangiocyte proliferation.

214 ness to kisspeptin, the main secretagogue of GnRH.

215 The expression and secretion of GnRH in NMC and isolated cholangiocytes was assessed.

216 a dual role of driving episodic secretion of GnRH through the differential release of peptide and ami

217 t individual cells are unreliable sensors of GnRH concentration and that this reliability is maximal

218 olog of human PROKR2) during early stages of GnRH neuronal migration.

219 As the most potent stimulator of GnRH/LH release, kisspeptin is believed to mediate the p

220 f human KISS1 and TAC3, 2 key stimulators of GnRH secretion.

221 ons important for generation of the surge of GnRH and LH that induces ovulation.

222 ve to positive feedback initiates a surge of GnRH release, culminating in ovulation.

223 SS1 receptor, KISS1R, is a potent trigger of GnRH secretion and inactivation of KISS1R on the GnRH ne

224 y and kisspeptin (KP) is a potent trigger of GnRH secretion from GnRH neurons.

225 f transcriptional factors acting upstream of GnRH.

226 ssed the stimulatory effect of kisspeptin on GnRH release in hypothalamic culture, GnIH had no inhibi

227 CVD risk was increased in men on GnRH agonists compared with the comparison cohort (hazar

228 by augmenting signaling via these pathways, GnRH secretion can be enhanced to treat some forms of in

229 During the juvenile period, GnRH neurons undergo morphological remodeling, concomita

230 t loss of tcf12 in zebrafish larvae perturbs GnRH neuronal patterning with concomitant attenuation of

231 experiments with varying near-physiological GnRH concentrations and pulse patterns.

232 nd positive feedback generating preovulatory GnRH/LH surges.

233 k mechanism responsible for the preovulatory GnRH surge.

234 ncrease firing rates during the preovulatory GnRH surge.

235 ed by blocking protein synthesis (to prevent GnRH from increasing DUSP expression) but did not differ

236 /PI3K signaling as a mechanism that prevents GnRH neuron deficiency.

237 g the KS-associated mutation did not protect GnRH neurons from death.

238 adiol induces negative feedback on pulsatile GnRH/luteinizing hormone (LH) release and positive feedb

239 the gonadotropin-releasing hormone receptor (GnRH-R).

240 the first EAP1 mutations leading to reduced GnRH transcriptional activity resulting in a phenotype o

241 act indirectly via KNDy neurons to regulate GnRH, the identity of upstream neurons that provide syna

242 We studied how estradiol feedback regulates GnRH excitability, a key determinant of neural firing ra

243 ey project to the median eminence to release GnRH.

244 mata of the neuroendocrine neurons releasing GnRH and controlling reproduction are located.

245 Cga expression, MSK1/2 inhibition repressed GnRH activation of Cga expression.

246 Current-clamp revealed GnRH neurons fired more action potentials in response to

247 H2) that specifically activates an A. rubens GnRH-type receptor and a novel neuropeptide (HNTFTMGGQNR

248 y onset and sexual reproduction by secreting GnRH to activate and maintain the hypothalamic-pituitary

249 tribution of solutions accounted for similar GnRH neuron excitability in all groups other than positi

250 velopment in the nasal mucosa and subsequent GnRH-1 neuronal migration.

251 Subsequently, GnRH receptor activation was completely abolished with a

252 Surprisingly, GnRH-1 neurogenesis was intact in Gli3(Xt/Xt) mice but t

253 ells coincident with production of sustained GnRH release that ultimately triggers ovulation.

254 We found that GnRH increases the levels of both modifications around t

255 ese observations support the hypothesis that GnRH neurons integrate fast-synaptic and intrinsic chang

256 We initially hypothesized that GnRH might induce phosphorylation of Ser-10 in histone 3

257 We have reported previously that GnRH-induced activities at these genes include various h

258 Moreover, ChIP analysis revealed that GnRH-activated MSK1 targets the first nucleosome just do

259 These data suggest that GnRH neurons integrate fast-synaptic and intrinsic chang

260 These data show for the first time that GnRH agonist treatment after puberty onset exerts sex-sp

261 The GnRH/GnRHR1 axis and miR-200b were up-regulated in human

262 owed a reduced ability to trans-activate the GnRH promoter compared to wild-type EAP1, due to reduced

263 neuropeptides dose-dependently activate the GnRH/AKH-like receptors GNRR-3 and GNRR-6 in a cellular

264 LUT1 expression increases in vivo during the GnRH-induced ovulatory LH surge and correlates with GnRH

265 Galphaq) was selectively inactivated in the GnRH neurons of global Gna11 (encodes Galpha11)-null mic

266 negative to positive feedback initiates the GnRH surge, ultimately triggering ovulation.

267 etwork that regulates the development of the GnRH axis.

268 sion are critical for the functioning of the GnRH neuron network in the female mouse.

269 emale puberty through transactivation of the GnRH promoter.

270 ereby confirming the Galphaq-coupling of the GnRH receptor in pituitary alphaT3-1 cells.

271 f hepatic fibrosis; however, the role of the GnRH/GnRHR1/miR-200b axis in the development of hepatic

272 secretion and inactivation of KISS1R on the GnRH neuron results in infertility.

273 that progesterone's inhibitory effect on the GnRH/LH surge and pulsatile secretion is mediated by its

274 speptin neurons are thought to represent the GnRH pulse generator, since their oscillatory activity i

275 Targeting the GnRH/GnRHR1/miR-200b axis may be key for the management

276 action of GnIH in GnRH neurons by using the GnRH neuronal cell line, GT1-7.

277 er to receive standard chemotherapy with the GnRH agonist goserelin (goserelin group) or standard che

278 multiple estrogen feedback loops within the GnRH neuronal network required for fertility in the fema

279 To resolve which components of this GnRH signal induce Fshb, we developed a high-throughput

280 Thus, GnRH nerve terminal function is controlled over disparat

281 3alpha in neurons or glial cells afferent to GnRH neurons.

282 cts that multiple combinations of changes to GnRH intrinsic conductances can produce the firing respo

283 ddress whether increased GABA innervation to GnRH neurons originates in the ARN, a viral-mediated Cre

284 alized tac3a-expressing cells in relation to GnRH and kisspeptin cells.

285 d from differential pituitary sensitivity to GnRH.

286 minish but not completely block KP-triggered GnRH secretion and that Galphaq/11-independent GnRH secr

287 lacking beta-arrestin-1 or -2, KP-triggered GnRH secretion is significantly diminished.

288 However, the mechanisms underlying GnRH pulse generation remain elusive.

289 tiated) compared with NLT (undifferentiated) GnRH neuronal cell lines.

290 e, buserelin) and 7.8 +/- 0.06 (pEC50 value, GnRH).

291 ary gonadotrope cells perifused with varying GnRH pulse frequencies.

292 status with input from the hypothalamus via GnRH receptor signaling to regulate reproductive hormone

293 At 2-3 weeks, GnRH release is suppressed before attaining adult patter

294 Moreover, while GnRH was expressed in both neuronal cell body and axons

295 rons heavily contacted and even bundled with GnRH neuron dendrites, and the density of fibers apposin

296 ammals via KNDy neurons and interaction with GnRH.

297 xpression, whereas continuous treatment with GnRH agonists upregulated Cga expression progressively a

298 Treatment with GnRH increased intrahepatic bile duct mass as well as pr

299 However, continuous treatment with GnRH stimulated LH secretion in vitro and in vivo, leadi

300 ndogenous GnRH and continuous treatment with GnRH, probably reflecting the status of Egr1 and Nr5a1 e