ライフサイエンスコーパス: NPY

1 NPY also acts in the mesolimbic dopaminergic circuitry,

2 NPY in the VTA was observed in fibers, but not following

3 NPY is prone to peptidolysis, generating metabolites wit

4 NPY is the prototype peptide that circulates in concentr

5 NPY neurons fire spontaneously, have a stellate morpholo

6 NPY, AGRP, CART, and pomc1a somata showed distribution p

7 NPY, via activation of Y5 receptors, additionally inhibi

8 NPY-saporin decreased spinal Y1R immunoreactivity but di

9 [ahx(5-24)]NPY also reduced tonic activation of GABA(B) receptors (

10 In tdT-Y(2)R mice, [ahx(5-24)]NPY increased excitability and suppressed the K(IR) in n

11 Y(2)R-expressing PNs responded to [ahx(5-24)]NPY with an enhancement of the I(sAHP) Ultimately, incre

12 that the selective Y(2)R agonist, [ahx(5-24)]NPY, reduced the frequency of GABA(A)-mediated mIPSCs in

13 ramethylrhodamine was linked to [F(7),P(34)]-NPY by amide or enzymatic linkage.

14 to the hY(1)R-preferring ligand [F(7),P(34)]-NPY by solid phase peptide synthesis.

15 nthesis and characterization of [F(7),P(34)]-NPY conjugates containing two methotrexate (MTX) molecul

16 ced at positions four and 22 of [F(7),P(34)]-NPY, connected by enzymatic or amide linkage.

17 ed intersectional genetic strategy to ablate NPY(+) noradrenergic neurons and/or adrenal chromaffin c

18 tor antagonist BIBO3304 completely abolished NPY effects on fear extinction retrieval.

19 Accordingly, NPY was shown to modulate cognitive functions in rodents

20 colocalized with cholinergic starburst ACs, NPY (neuropeptide Y)- and EBF1 (early B-cell factor 1)-p

21 High-intensity ES at the abdomen activates NPY(+) splenic noradrenergic neurons via the spinal-symp

22 4 (DPP4)/CD26 by endothelial cells activates NPY-mediated signaling by increasing the bioavailability

23 lity of AgRP neurons to signal through AgRP, NPY, or GABA, and then stimulated these cells using a pa

24 When AgRP/NPY neurons are inactivated, ARC glial activation fails

25 Here, we show that enzymatically altered NPY signaling in ECs caused reduced VE-cadherin and CD31

26 Although NPY has potent anxiolytic actions within the BLA, select

27 modulation by NPY in the IL cortex, although NPY and NPY receptors are abundant in these areas.

28 Here we identify an NPY/neuropeptide F (NPF)-related neuropeptide system in

29 eurons with intrathecal administration of an NPY-conjugated saporin ribosomal neurotoxin that spares

30 Second, nanoinjections of NPY or an NPY receptor Y1 (NPY1R) antagonist into PVN or DMH decre

31 nclude the orexigenic neuropeptides AgRP and NPY for specifying AgRP-neurons, the anorexigenic neurop

32 s of the Gi-coupled micro opioid, GABA-B and NPY receptors.

33 Fasting dramatically increased cFos- and NPY-immunoreactivity in the IN, followed by rapid reduct

34 Double-labeling with CTB and NPY was observed in the Arc and in the ventrolateral med

35 lass of inhibitory neurons that use GABA and NPY signaling to regulate activity in the IC and auditor

36 ns that are well poised to use GABAergic and NPY signaling to regulate the excitability of circuits i

37 fic nuclei; (b) in course of aging, HCRT and NPY expressing neurons are localized also in telencephal

38 cursor is also known as hypocretin-HCRT) and NPY, and their regulation by food intake in the short-li

39 diated in the CA1 region of hippocampus, and NPY injection into hippocampus alleviates anxiety sympto

40 es by releasing primarily norepinephrine and NPY.

41 on by NPY in the IL cortex, although NPY and NPY receptors are abundant in these areas.

42 Neuropeptide Y (NPY) and NPY receptors represent a highly conserved, stress-activ

43 elty in the study of central orexinergic and NPY-ergic systems in vertebrates', demonstrating an unco

44 e specimens, show that: (a) HCRT and OXA and NPY mRNA and protein are localized in neurons of diencep

45 thylation levels of 3 genes (Wif1, PENK, and NPY) were shown closely associated with CRC dysbiosis.

46 rons, plateau low threshold spike (PLTS) and NPY-neurogliaform (NGF) cells.

47 We hypothesize that POMC and NPY/AgRP cell fates are specified and maintained by dist

48 orly studied.SIGNIFICANCE STATEMENT POMC and NPY/AgRP neurons are derived from the same hypothalamic

49 ed the transcriptomes of developing POMC and NPY/AgRP neurons in mice.

50 ir opposing actions on food intake, POMC and NPY/AgRP neurons in the arcuate nucleus of the hypothala

51 anscriptomes of genetically labeled POMC and NPY/AgRP neurons in the developing mouse hypothalamus to

52 Likewise, TH and NPY were colocalized in noradrenergic nerves throughout

53 In comparison, VGLUT1 and NPY immunoreactivities were not altered.

54 sidering that chronic obesity decreases ArcN NPY content, we propose that the ArcN NPY neuropathway t

55 DDs) to selectively activate or inhibit ArcN NPY neurons expressing agouti-related peptide (AgRP) in

56 elective, DREADD-mediated activation of ArcN NPY/AgRP neurons.

57 Finally, stimulation of ArcN NPY/AgRP terminal fields in the PVN and DMH decreased SS

58 First, we found that ArcN NPY/AgRP fibers closely appose PVN and DMH presympatheti

59 s ArcN NPY content, we propose that the ArcN NPY neuropathway to the PVN and DMH is pivotal in obesit

60 revents acyl-ghrelin from activating arcuate NPY neurons.

61 A high-fat diet did not alter arcuate NPY neuronal InsR expression in males or females.

62 dy, we examined whether Abeta causes arcuate NPY neuronal dysfunction by disrupting intracellular Ca(

63 were not associated with changes in arcuate NPY neuronal insulin receptor expression.

64 e the intracellular Ca(2+) levels in arcuate NPY neurons from Tg2576 brain slices.

65 hicine treatment or 24 hr fasting, to assess NPY/Npy expression locally in the VTA.

66 The TGF-beta/NPY/Y5R axis and DPP4 represent attractive therapeutic t

67 within the BLA, selective activation of BLA NPY Y(2) receptors (Y(2)Rs) acutely increases anxiety by

68 (2)Rs.SIGNIFICANCE STATEMENT Within the BLA, NPY is potently anxiolytic.

69 TH-MYCN mice, high immunoreactivity of both NPY and Y5R marked angioinvasive NB cells.

70 king memory performance were not affected by NPY infusion into the IL.

71 n be interrupted by neuromodulation, here by NPY via Y(2)Rs.SIGNIFICANCE STATEMENT Within the BLA, NP

72 No information exists on fear modulation by NPY in the IL cortex, although NPY and NPY receptors are

73 -stimulated feeding, and this was rescued by NPY re-expression selectively in AgRP neurons.

74 a physiologically derived spike train causes NPY release that reduces short-term facilitation, wherea

75 abundant in perisomatic synapses of CCK(+) , NPY(+) /SOM(+) , and vAChT(+) interneurons.

76 of aging nor by food intake; and (e) central NPY levels are augmented in course of aging, and regulat

77 It further suggests that the central NPY system exerts differential effects on the sequential

78 statin interneurons, some of which coexpress NPY.

79 signals through its evolutionarily conserved NPY/NPF GPCR, NPR-11, in downstream AIA interneurons.

80 arization and perivascular fibers containing NPY.

81 interneurons expressing neuropeptide Y::Cre (NPY(+)) in the dorsal spinal cord.

82 Hepatocyte-derived NPY promoted HCC progression by Y5R activation.

83 This method was able to detect NPY without performing a redox reaction by adsorption at

84 d confocal microscopy were used to determine NPY-immunoreactive afferents to the VTA.

85 is conferred by three functionally distinct NPY+ cell types, with differences in intrinsic excitabil

86 nce immunoassays are not able to distinguish NPY from its metabolites, we have validated a microliqui

87 The Caenorhabditis elegans NPY/NPF ortholog FLP-34 displays conserved structural ha

88 Endogenous NPY in the NAc originates from local interneurons and af

89 w therapeutic targets to increase endogenous NPY release in patients in a spatially and temporally ap

90 However, the origin of endogenous NPY in the VTA is unknown.

91 t stress abolishes the release of endogenous NPY onto temporoammonic synapses, a stress-sensitive pat

92 unction through the impairment of endogenous NPY release, potentially contributing to heightened anxi

93 ) assay for the quantification of endogenous NPY, NPY2-36, NPY3-36, NPY1-35, and NPY3-35 in human pla

94 hippocampal slices from mice that endogenous NPY, released in response to optogenetic stimulation or

95 These data establish NPY as an important vertebrate sleep/wake regulator and

96 dings suggest a pathogenic role of excessive NPY-NPY2R signaling in the glomerulus and that inhibitin

97 ostaining confirmed that NPY neurons express NPY, and we therefore hypothesized that NPY signaling re

98 In obese females, NPY inhibition in the PVN was maintained.

99 ans foraging decisions NPR-1 and TYRA-3, for NPY-like neuropeptides and tyramine respectively, do not

100 These findings reveal a unique role for NPY in sustaining hunger in the interval between food di

101 ively, our data suggest a potential role for NPY, AGRP, POMC, and CART in regulating energetic status

102 tivation of nicotinic receptors on GABAergic NPY-neurogliaform interneurons that monosynaptically inh

103 tion was provided by the expression of Gbx2, NPY, Lhx1, and Lhx9.

104 proteomic analysis revealed that glomerular NPY-NPY2R signaling predicted nephrotoxicity, modulated

105 ound that head motion was greater among High-NPY subjects, consistent with previous reports linking N

106 extremes of NPY expression (Low-NPY and High-NPY) to participate in functional magnetic resonance ima

107 reater for Low-NPY subjects relative to High-NPY subjects, regardless of stimulus valence.

108 eptors at multiple sites in the dorsal horn: NPY Y1 receptors (Y1Rs) on post-synaptic neurons and bot

109 To determine how NPY regulates sleep, we tested for interactions with sev

110 on and discovered that drugs targeting human NPY receptors modulate mosquito host-seeking.

111 Ae. aegypti peptide receptors, we identified NPY-like receptor 7 (NPYLR7) as the sole target of these

112 s), guiding the assembly of a functional IGL(NPY)-SCN circuit.

113 express neuropeptide Y (NPY) (hereafter, IGL(NPY) neurons), guiding the assembly of a functional IGL(

114 ostnatal stages, and acute inhibition of IGL(NPY) terminals in the SCN decreased food-anticipatory ac

115 Moreover, silencing IGL(NPY) neurons in adult mice mimicked the deficits that we

116 in the early postnatal period tunes the IGL(NPY)-SCN circuit to allow entrainment to time-restricted

117 This study shows that IL NPY inhibits consolidation of extinction, resulting in i

118 ) was enriched in POMC neurons but absent in NPY/AgRP neurons.

119 energy balance is associated with changes in NPY and OX in a region-specific manner.

120 and implicate sexually dimorphic changes in NPY inhibition of SNA in the PVN as one mechanism.

121 in obese males as a result of a decrease in NPY inputs.

122 e possibility that individual differences in NPY expression moderate the risk for disorders of mesoac

123 alpha1A - and beta- adrenergic receptors in NPY/AgRP neurons, while POMC neurons are inhibited via a

124 d the impact of stress-induced reductions in NPY on circuit function, are unknown.

125 Mechanistically, the lack of Snord116 in NPY neurons leads to the upregulation of NPY mRNA consis

126 naling in the glomerulus and that inhibiting NPY-NPY2R signaling in albuminuric kidney disease has th

127 population remains sensitive to intrathecal NPY after nerve injury.

128 Gravid females also had larger NPY and AGRP neurons in the NLT compared to brooding fem

129 Furthermore, we found that its ligand NPY was secreted by peritumorous hepatocytes.

130 ant vertebrate sleep/wake regulator and link NPY signaling to an established arousal-promoting system

131 provide the first evidence in humans linking NPY with salience sensitivity of the NAc, raising the po

132 ts, consistent with previous reports linking NPY with hyperactivity.

133 n rodent models, and naturally occurring low NPY expression in humans has been associated with negati

134 jects at the extremes of NPY expression (Low-NPY and High-NPY) to participate in functional magnetic

135 us low-salience stimuli were greater for Low-NPY subjects relative to High-NPY subjects, regardless o

136 signaling functions of NPF and its mammalian NPY homolog in drug and alcohol disorders, these observa

137 In brain slice recordings, many NPY neurons fired spontaneously, suggesting that NPY neu

138 SPC trafficking and identify a CD26-mediated NPY axis that has potential as a pharmacologic target to

139 lpha-klotho, negated its ability to modulate NPY/AgRP neurons, and blunted its therapeutic effects.

140 Nonbreeding birds had more NPY immunoreactivity, specifically in three brain region

141 Moreover, NPY conversion by dipeptidylpeptidase 4 (DPP4) augmented

142 Moreover, NPY neurons in the arcuate nucleus became resistant to t

143 Thus, larger appetite-stimulating neurons (NPY, AGRP) likely promote feeding while females are grav

144 No NPY- or Npy-expressing cell bodies were observed in the

145 in OP females, suggesting that with obesity NPY neurons become resistant to the inhibitory effects o

146 Here we showed that the ability of NPY on C-Fos induction in the PVH was blunted in conditi

147 ar mechanisms associated with the actions of NPY.

148 However, selective activation of NPY(2) receptors (Y(2)Rs) increases anxiety by an unknow

149 Moreover, the adsorption of NPY to the aptamer-modified microelectrodes was also dem

150 Carriers of NPY gene polymorphism rs16147 have been reported to have

151 ar gateway specifically opens by cleavage of NPY by CD26 signaling via NPY2 and NPY5 receptors.

152 We also showed that the concentrations of NPY and its metabolites are similar in healthy volunteer

153 critical role of Snord116 in the control of NPY neuronal functions that might be dysregulated in PWS

154 Deletion of NPY, but not AgRP or GABA, abolished optically-stimulate

155 Thus, widespread CNS-targeted delivery of NPY appears to be effective at reversing the neuronal an

156 ons are stellate cells, and the dendrites of NPY neurons in the tonotopically organized central nucle

157 tigated possible memory-enhancing effects of NPY and determined the role of the NPY system in the acq

158 Anxiolytic effects of NPY are mediated in the CA1 region of hippocampus, and N

159 in the long-term, anxiolytic-like effects of NPY in the BLA, consistent with an intrinsic role in str

160 ween the molecular and behavioral effects of NPY.

161 cted 53 of these subjects at the extremes of NPY expression (Low-NPY and High-NPY) to participate in

162 the bioavailability of the truncated form of NPY.

163 lite to understand the multiple functions of NPY.

164 e nucleus accumbens (NAc), but the impact of NPY on the human NAc is largely unexplored.

165 Intracerebroventricular (icv) infusion of NPY (1 nmol/2 microl) prolonged retention of non-social

166 While icv infusion of NPY did not affect the acquisition, consolidation, and r

167 Infusion of NPY into the IL cortex in rats significantly impaired fe

168 Finally, repeated intra-BLA injections of NPY or a Y(5) receptor agonist increased social interact

169 a condition associated with a high level of NPY and a low level of insulin.

170 h the increased plasma and urinary levels of NPY that are observed in such conditions.

171 iptome/genome sequence data revealed loss of NPY/NPF-type signalling, but orthologs of PrRP-type neur

172 range was obtained from 10 to 1000 ng/mL of NPY.

173 ho/FGFR1/PI3K signaling in the modulation of NPY/AgRP neuron activity and maintenance of energy homeo

174 Yet, PVN nanoinjections of NPY decreased LSNA similarly between groups.

175 Second, nanoinjections of NPY or an NPY receptor Y1 (NPY1R) antagonist into PVN or

176 Here we investigated the occurrence of NPY/NPF/PrRP/sNPF-related signalling systems in a deuter

177 We show that overexpression of NPY increases sleep, whereas mutation of npy or ablation

178 e orthologous and originated as a paralog of NPY/NPF-type signalling in Urbilateria.

179 F (sNPF) have been identified as paralogs of NPY/NPF in vertebrates and protostomes, respectively.

180 rvations raise the intriguing possibility of NPY-related transgenerational effects in humans.

181 ied affinity for the five known receptors of NPY that mediate distinct effects.

182 TGF-beta1 was identified as a regulator of NPY in hepatocytes and induced Y5R in invasive cancer ce

183 rt-term facilitation, whereas the release of NPY that modulates Schaffer collateral synapses requires

184 sociations, a process that is reminiscent of NPY signaling in mammals.

185 However, the role of NPY signaling in the medial prefrontal cortex (mPFC), wh

186 Pathway specificity of NPY release is conferred by three functionally distinct

187 timulation or synaptically evoked spiking of NPY+ cells, suppresses both of the feedforward pathways

188 s article also advances the understanding of NPY+ cells and the factors that regulate their spiking,

189 in NPY neurons leads to the upregulation of NPY mRNA consistent with the hyperphagic phenotype and s

190 ing anti-inflammatory effects that depend on NPY(+) adrenal chromaffin cells.

191 First, the impact of DID on NPY immunoreactivity (IR) was assessed in the mPFC.

192 Mice lacking CD26 or NPY exhibited impaired HSPC trafficking that was restore

193 s, increasing the activity of the orexigenic NPY/AgRP neurons and decreasing the activity of the anor

194 r the anorexigenic (POMC) or the orexigenic (NPY/AgRP) identity remains elusive.

195 ue as it prefers pancreatic polypeptide over NPY and peptide YY.

196 erve injury (SNI) model of neuropathic pain, NPY-saporin decreased mechanical and cold hypersensitivi

197 blood vessels and neurons, and in particular NPY and POMC neurons in the arcuate nucleus.

198 al gene promoters including SFRP1,2,3, PENK, NPY, ALX4, SEPT9, and WIF1 promoters were found hypermet

199 ulate neuropeptide Y/agouti-related peptide (NPY/AgRP)-expressing neurons, energy balance, and glucos

200 We synthesized a series of peptidic NPY Y(4)R ligands, derived from the hexapeptide acetyl-A

201 In vitro, podocyte NPY signaling occurred via the NPY2 receptor (NPY2R), st

202 ve been reported to have elevated prefrontal NPY expression.

203 , while a Y(5) receptor antagonist prevented NPY's effects both on behavior and on structure.

204 enic (neuropeptide Y/agouti-related protein; NPY/AgRP) and anorexigenic (proopiomelanocortin; POMC) n

205 However, PVN NPY injection decreased LSNA similarly in obesity prone/

206 In males, blockade of PVN NPY Y1 receptors with BIBO3304 increased LSNA in CON/OR

207 Thus, tonic PVN NPY inhibition of LSNA may be lost in obese males as a r

208 protein-coupled neuropeptide Y Y2 receptor (NPY(2)R) and serotonin 5-hydroxytryptamine (HT)(2C) rece

209 The recombinant NPY-apoB effectively reversed neurodegenerative patholog

210 Three, 4-day cycles of DID reduced NPY IR in the mPFC.

211 e that (1) binge-like ethanol intake reduces NPY levels in the mPFC; (2) activation of NPY1R or block

212 The mechanisms that regulate NPY release, and its effects on CA1 synaptic function, a

213 The effects of endogenously released NPY during physiologically relevant stimulation, and the

214 In organotypic slice cultures, repeated NPY treatment reduces the complexity of the dendritic ex

215 characterized persistent effects of repeated NPY and CRF treatment on the structure and function of B

216 principal neurons within the OTCs, repeated NPY treatment caused persistent attenuation of excitator

217 Elevated serum NPY levels correlated with an adverse clinical presentat

218 , and examined the contributions of specific NPY receptor subtypes to these neural and behavioral eff

219 Studying NPY-knockout mice, we found that NPY deficiency in vivo

220 alysis revealed that alpha-klotho suppresses NPY/AgRP neuron activity, at least in part, by enhancing

221 ating peptide in resting conditions and that NPY and catecholamines are simultaneously increased duri

222 Immunostaining confirmed that NPY neurons express NPY, and we therefore hypothesized t

223 in rodent models have also demonstrated that NPY elicits reward behaviors through its action in the n

224 By demonstrating that NPY release modulates hippocampal synaptic plasticity an

225 , genetic, and pharmacological evidence that NPY promotes sleep by inhibiting noradrenergic signaling

226 tions provide the first direct evidence that NPY signaling in the mPFC modulates binge-like ethanol c

227 Studying NPY-knockout mice, we found that NPY deficiency in vivo surprisingly reduced the level of

228 Additionally, we found that NPY signaling hyperpolarized the membrane potential of a

229 e) and Ai14 Cre-reporter mice, we found that NPY Y(1) receptor (Y(1)R)-expressing neurons are glutama

230 ress NPY, and we therefore hypothesized that NPY signaling regulates activity in the IC.

231 y analyzing sleep architecture, we show that NPY regulates sleep primarily by modulating the length o

232 Retrograde tracing showed that NPY neurons are principal neurons that can project to th

233 Morphologic reconstructions showed that NPY neurons are stellate cells, and the dendrites of NPY

234 Collectively, these results suggest that NPY inputs were decreased.

235 neurons fired spontaneously, suggesting that NPY neurons may drive tonic inhibition onto postsynaptic

236 This study suggests that NPY has memory-enhancing effects in a non-social context

237 The NPY Y1 receptor antagonist BIBO3304 completely abolished

238 EGR1 also bound the NPY receptor Y1 gene (Npy1r), which co-occurred with sex

239 et of excitatory IC neurons that express the NPY Y(1) receptor.

240 tic target for advanced NB and implicate the NPY/Y5R axis in disease dissemination.

241 SNPs in the NPY, IL37, and NCR2 genes were associated with susceptib

242 ffects of NPY and determined the role of the NPY system in the acquisition, consolidation, and retrie

243 This NPY-mediated neuroplasticity indicates that resilience o

244 Thus, NPY dampens excitability of IL projection neurons and im

245 Thus, NPY neurons are a novel class of inhibitory neurons that

246 Thus, NPY neurons represent a novel class of inhibitory princi

247 The rs2521634-AA (close to NPY gene) presented increased risk for severe periodonti

248 These structural responses to NPY or CRF required calcineurin or CaMKII, respectively.

249 hat was restored by treatment with truncated NPY.

250 P), substance P (SP), neuropeptide tyrosine (NPY), and the nitric oxide synthesizing enzyme neuronal

251 Our findings validate NPY as a therapeutic target for advanced NB and implicat

252 eight male Wistar rats, if the source of VTA NPY is local, and/or whether it is derived from VTA-proj

253 Thus, VTA NPY originates from the hypothalamic Arc and the ventrol

254 f old animals and in fasted animals, whereas NPY increased sharply; (d) central HCRT levels are not r

255 wever, the sites and neurocircuitry by which NPY decreases SNA are unclear.

256 However, the mechanisms by which NPY modulates circuit function to reduce anxiety behavio

257 lucidate the neural mechanisms through which NPY influences NAc function and related behaviors.

258 rved structural hallmarks of bilaterian-wide NPY/NPF neuropeptides.

259 Repeated treatment of OTCs with NPY followed by an identical treatment with CRF, or vice

260 ces IGL neurons that express neuropeptide Y (NPY) (hereafter, IGL(NPY) neurons), guiding the assembly

261 asoconstrictive mechanism as Neuropeptide Y (NPY) acting on Y1 receptors.

262 ved form of neurotransmitter neuropeptide Y (NPY) actively promotes a breach of BM vascular sinusoida

263 Endogenous neuropeptide Y (NPY) and corticotrophin-releasing factor (CRF) modulate

264 Neuropeptide Y (NPY) and its receptors (especially Y1, Y2, and Y5) are h

265 Neuropeptide Y (NPY) and NPY receptors represent a highly conserved, str

266 rculating steroids, and both neuropeptide Y (NPY) and orexin (OX) immunoreactivity.

267 Orexin A (OXA) and neuropeptide Y (NPY) are two hypothalamic neuropeptides involved in the

268 report the identification of neuropeptide Y (NPY) as both necessary for normal daytime sleep duration

269 The hypothalamic neuropeptide Y (NPY) circuitry is a key regulator of feeding behavior.

270 Endogenous neuropeptide Y (NPY) exerts long-lasting spinal inhibitory control of ne

271 We found that neuropeptide Y (NPY) expression identifies a class of GABAergic principa

272 of both sexes, we found that neuropeptide Y (NPY) expression identifies a major class of inhibitory n

273 Neuropeptide Y (NPY) has robust anxiolytic properties and is reduced in

274 SIGNIFICANCE STATEMENT: Neuropeptide Y (NPY) has robust anxiolytic properties, and its levels ar

275 n tonic inhibition of SNA by neuropeptide Y (NPY) in the paraventricular nucleus (PVN).

276 tonic inhibition of LSNA by neuropeptide Y (NPY) in the PVN.

277 two populations of striatal neuropeptide Y (NPY) interneurons, plateau low threshold spike (PLTS) an

278 Neuropeptide Y (NPY) is a 36-amino acid peptide circulating at a subpico

279 basolateral amygdala (BLA), neuropeptide Y (NPY) is associated with buffering the neural stress resp

280 Here we show that Neuropeptide Y (NPY) is uniquely required for the long-lasting effects o

281 Among them, neuropeptide Y (NPY) is well known to promote aversive memory acquisitio

282 ICV TTR decreased neuropeptide Y (NPY) levels in the DMH and the paraventricular nucleus (

283 Neuropeptide Y (NPY) produces anxiolytic effects in rodent models, and n

284 Within the family of neuropeptide Y (NPY) receptors, the Y(4) receptor (Y(4)R) is unique as i

285 Neuropeptide Y (NPY) signaling via limbic NPY1 and 2 receptors (NPY1R an

286 ltaneous withdrawal of tonic neuropeptide Y (NPY) sympathoinhibition.

287 We found that Neuropeptide Y (NPY) was significantly down-regulated in insulin-resista

288 Neuropeptide Y (NPY), a 36 aa peptide, regulates stress and emotional be

289 ious studies have identified neuropeptide Y (NPY), a sympathetic neurotransmitter expressed in NB, as

290 nhibits food intake, whereas neuropeptide Y (NPY), a well-known orexigenic peptide, stimulates it.

291 of these neuron also express neuropeptide Y (NPY), and this coexpression is maintained by dissociated

292 he neuropeptides galanin and neuropeptide Y (NPY), brain-derived neurotrophic factor (BDNF), as well

293 One relevant target is neuropeptide Y (NPY), which regulates both stress and food-intake.

294 Abeta causes dysfunction in neuropeptide Y (NPY)-expressing hypothalamic arcuate neurons before plaq

295 687-701) determined that the neuropeptide Y (NPY)-like receptor 7 (NPYLR7) controls mosquito satiety

296 We investigated a role for neuropeptide Y (NPY)-related signaling in long-term behavioral suppressi

297 uncates the neurotransmitter neuropeptide Y (NPY).

298 Orthologs of vertebrate neuropeptide-Y (NPY) known as neuropeptide-F (NPF) have been identified

299 calize appetite-stimulating (neuropeptide Y, NPY; agouti-related protein, AGRP) and appetite-inhibiti

300 that is only visible after inhibition of Y1 NPY receptors.