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 induced a modest increase in Homer1b/c expression a

4 GnRH neuron deficiency in male mice was accompanied by i

5 GnRH neurons are initially activated in utero but remain

6 GnRH neurons do not express the estrogen receptor needed

7 GnRH receptor subtypes GnRHR1 and GnRHR2 were expressed

8 GnRH regulates the pituitary gonadotropin's follicle-sti

9 GnRH regulation of GDF9 was concentration-dependent and

10 GnRH secreted by cholangiocytes promotes biliary prolife

11 GnRH-induced biliary proliferation was evaluated by chan

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

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

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

15 growth differentiation factor 9 (GDF9) as a GnRH-suppressed autocrine inducer of FSHbeta gene expres

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

17 R, identified in the heterozygous state in a GnRH-deficient patient, also interfered with dissociatio

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

19 Administration of a GnRH analog to rats leads to similar degenerative neurop

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

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

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

23 ated virus into the median eminence of adult GnRH-Cre mice resulted in the selective expression of Ch

24 analyzed for zonulin and antibodies against GnRH and luteinizing hormone, and their receptors.

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

26 at the SGK-1 gene is up-regulated by Dex and GnRH alone, whereas a combination of both ligands result

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

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

29 FSHbeta mRNA induction by GDF9 and GnRH was synergistic.

30 Here, we investigated GR and GnRH receptor (GnRHR) cross-talk that involves co-locali

31 e neural circuits between ARC kisspeptin and GnRH neurons are fully established and operative before

32 ed the expression variation of RFRP mRNA and GnRH mRNA in the hypothalamus from hamsters with differe

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

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

35 This effect is indirect, as GnRH neurons do not express leptin receptors (LEPRs).

36 prostate cancer than the currently available GnRH agonists.

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

38 actually resulted from variations in average GnRH concentration.

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

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

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

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

43 g regulator SRp20 was found to be induced by GnRH.

44 te that the regulation of Homer1 splicing by GnRH contributes to gonadotropin gene control.

45 a global regulation of pre-mRNA splicing by GnRH.

46 eover, loss-of-function NK3R mutations cause GnRH deficiency in humans.

47 thway for GnRH neurons, in FEZF1 deficiency, GnRH neurons also fail to enter the brain.

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

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

50 knockdown on FSHbeta induction at different GnRH pulse frequencies using a parallel perifusion syste

51 Driving GnRH neurons to exhibit simultaneous burst firing was in

52 hematical and biochemical basis of a dynamic GnRH signaling system that is robust to changes in pulse

53 this study on rat was to evaluate the early GnRH-induced enteric neuropathy in terms of distribution

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

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

56 with an opportunity to visualize the entire GnRH system simultaneously in one organism.

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

58 s with the onset of the ability of exogenous GnRH to induce pituitary LH secretion.

59 xperiments demonstrated that ChR2-expressing GnRH neurons could be driven to fire with high spike fid

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

61 in these tracks is the migratory pathway for GnRH neurons, in FEZF1 deficiency, GnRH neurons also fai

62 e preferentially decreased by high frequency GnRH pulses.

63 Early high-frequency GnRH release was similar in wild-type and kisspeptin kno

64 oxical induction of FSHbeta by low frequency GnRH pulses are incompletely understood.

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

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

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

68 peptin receptor was deleted selectively from GnRH neurons.

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

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

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

72 ,959 were on gonadotropin-releasing hormone (GnRH) agonists, and 3,747 underwent surgical orchiectomy

73 treated with gonadotropin-releasing hormone (GnRH) analogs may develop enteric neuropathy and dysmoti

74 Both gonadotropin-releasing hormone (GnRH) and activins, members of the transforming growth f

75 a signaling, gonadotropin-releasing hormone (GnRH) and epidermal growth factor receptor family (ErbB)

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

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

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

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

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

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

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

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

84 Gonadotropin-releasing hormone (GnRH) is secreted in brief pulses from the hypothalamus

85 Gonadotropin-releasing hormone (GnRH) is secreted in brief pulses that stimulate synthes

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

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

88 y shown that gonadotropin-releasing hormone (GnRH) ligand-independently activates the GR and synergis

89 n to inhibit gonadotropin-releasing hormone (GnRH) neuronal activity and hence reproduction in birds

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

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

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

93 Gonadotropin-releasing hormone (GnRH) neurons are neuroendocrine cells, located in the h

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

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

96 ivity of the gonadotropin-releasing hormone (GnRH) neurons in vivo to establish the minimal parameter

97 Gonadotropin-releasing hormone (GnRH) neurons originate outside the CNS in the olfactory

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

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

100 stimulating gonadotropin-releasing hormone (GnRH) neurons via the kisspeptin receptor KISS1R.

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

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

103 g from mouse gonadotropin-releasing hormone (GnRH) neurons.

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

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

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

107 Hypothalamic gonadotropin-releasing hormone (GnRH) plays a critical role in reproductive physiology b

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

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

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

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

112 e pattern of gonadotropin-releasing hormone (GnRH) secretion from the CNS is a hallmark of the pubert

113 Gonadotropin-releasing hormone (GnRH) secretion is regulated by estradiol feedback.

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

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

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

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

118 ns secreting gonadotropin-releasing hormone (GnRH), the neuropeptide controlling reproduction.

119 by secreting gonadotropin-releasing hormone (GnRH).

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

121 particular, gonadotropin replacing hormone (GnRH) is released in rhythmic pulses, and disruption of

122 ese observations provide an insight into how GnRH neurons generate pulsatile LH secretion in vivo.

123 ctive expression of ChR2 in hypophysiotropic GnRH neurons.

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

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

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

127 rhythmic oscillations in internal pH and in GnRH delivery over a period of one week.

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

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

130 identified second CXCL12 receptor, CXCR7, in GnRH neuron development.

131 Information could be encoded in GnRH pulse frequency, width, amplitude, or other feature

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

133 ling and the conditional deletion of Nrp1 in GnRH neurons counteract Sema3A-induced axonal sprouting.

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

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

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

137 not directly inhibit kisspeptin signaling in GnRH neurons.

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

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

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

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

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

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

144 Homer1 gene knockdown resulted in increased GnRH-induced FSHbeta and LHbeta transcript levels.

145 Kisspeptin increased GnRH excitability and was essential for estradiol regula

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

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

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

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

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

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

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

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

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

155 Interestingly, GnRH neurons in adult animals are multiciliated and the

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

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

158 sing a lineage switch of ectopically located GnRH neurons.

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

160 le-like brain characteristics in adult male, GnRH receptor knock-out mice.

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

162 significant reduction in kisspeptin-mediated GnRH neuronal activity.

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

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

165 After migrating, GnRH neurons are located in the hypothalamus and are ess

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

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

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

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

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

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

172 Optogenetic activation of GnRH neurons for 30-s to 5-min time periods over a range

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

174 e result was found for optical activation of GnRH projections in the median eminence.

175 uropeptide kisspeptin, a potent activator of GnRH neurons that is implicated as a critical permissive

176 dentified to be potent, direct activators of GnRH neurons.

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 chanisms underlying developmental control of GnRH neuron activity remain unknown.

184 implicated in the neuroendocrine control of GnRH release; however, little is known about the structu

185 ron," greatly expands the dynamic control of GnRH secretion into the pituitary portal system to regul

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

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

188 Homer1b/c ratio and modulated the effects of GnRH on FSHbeta and LHbeta expression.

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

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

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

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

195 Imaging of GnRH neurons revealed greater dendritic spine density th

196 Additionally, the investigation of GnRH expression level showed a declining expression tren

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

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

199 of pituitary secretory response, not lack of GnRH release, initially blocks downstream activation of

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

201 ng hormone secretion (an indirect measure of GnRH neuron activity) but is required for regulation of

202 s of Nscl-2 results in aberrant migration of GnRH neurons in Nscl-2 mutant mice causing a lineage swi

203 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

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

205 The necessity of GnRH signaling for the sexually differentiating effects

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

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

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

209 mals are multiciliated and the percentage of GnRH neurons possessing multiple Kiss1r-positive cilia i

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

211 Premature reactivation of GnRH neurons results in precocious puberty in mice and h

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

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

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

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

216 ness to kisspeptin, the main secretagogue of GnRH.

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

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

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

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

221 lready communicate with a specific subset of GnRH neurons in utero.

222 ons important for generation of the surge of GnRH and LH that induces 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 that ARC kisspeptin neurons are upstream of GnRH neurons, and that GnRH neuron connectivity to ARC k

226 optical fibers implanted in the vicinity of GnRH neurons within the rostral preoptic area.

227 as considered as a hypothetical inhibitor on GnRH, shows a stimulatory effect on the male Syrian and

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

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

230 markably, disruption of cilia selectively on GnRH neurons leads to a significant reduction in kisspep

231 ocrine integration, and immune inhibition or GnRH restoration in the hypothalamus/brain represent two

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

233 tions demonstrate the necessity of perinatal GnRH signaling for driving brain sexual differentiation

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

235 einizing hormone surge, likely by perturbing GnRH release into the hypothalamo-hypophyseal portal sys

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

237 Finally, we show that Dex plus GnRH synergistically inhibit cell proliferation in a man

238 k mechanism responsible for the preovulatory GnRH surge.

239 ribute to the generation of the preovulatory GnRH surge.

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

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

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

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

244 nadotropin-inhibitory hormone (GnIH) reduced GnRH release frequency in slices from 1-week-old mice.

245 ar region (AVPV) may differentially regulate GnRH neurons during negative and positive feedback, resp

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

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

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

249 RF9, a putative GnIH antagonist, restored GnRH release in slices from testosterone-treated mice, s

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

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

252 to detect directly the oxidation of secreted GnRH.

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

254 Reduction in early life spontaneous GnRH release frequency coincides with the onset of the a

255 We studied spontaneous GnRH secretion in brain slices from male mice during per

256 Subsequently, GnRH receptor activation was completely abolished with a

257 on in response to activation of cell surface GnRH receptors.

258 y more important roles in FSH synthesis than GnRH.

259 urons are upstream of GnRH neurons, and that GnRH neuron connectivity to ARC kisspeptin neurons does

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

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

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

263 They reveal that GnRH neurons in vivo exhibit considerable heterogeneity

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

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

266 SRp20 depletion attenuated the GnRH-induced increase in the Homer1a-to-Homer1b/c ratio

267 nse kinetics lead to ERK activity beyond the GnRH pulse, and this reduces sensitivity to pulse width.

268 Forty rats were given the GnRH analog buserelin (20 mug, 1 mg/ml) or saline subcut

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

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

271 The caudal-most extension of the GnRH neuron continuum brings some cells very close to th

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

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

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

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

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

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

278 tributes to a regulatory loop that tunes the GnRH frequency-response characteristics of the FSHbeta g

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

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

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

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

283 Thus, GnRH nerve terminal function is controlled over disparat

284 In addition to GnRH neurons, KISS1R is expressed in other brain areas a

285 3alpha in neurons or glial cells afferent to GnRH neurons.

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

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

288 ation and indicate that kisspeptin inputs to GnRH neurons are essential for this process to occur.

289 The importance of kisspeptin inputs to GnRH neurons for the process of sexual differentiation w

290 d from differential pituitary sensitivity to GnRH.

291 Limiting the leptin-to-GnRH mediators to GABAergic cells will enable future res

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

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

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

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

296 ary gonadotrope cells perifused with varying GnRH pulse frequencies.

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

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

299 3R we previously identified in patients with GnRH deficiency, we demonstrate that Y256H and Y315C NK3

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