ライフサイエンスコーパス: NPY

1 NPY induces abundant expression of C-Fos, an indicator f

2 NPY innervation of the BLA was assessed in rats by exami

3 NPY is an especially significant biomarker, since it can

4 NPY reduces neuronal firing in the Acb resulting in incr

5 NPY strongly decreased stimulation-induced EPSPs in dent

6 NPY(-/-) mice had increased incidence and kinetics of re

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

8 e neuropeptide Y (NPY) analogue [F(7),P(34)]-NPY as targeting moiety are able to deliver toxic agents

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

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

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

12 y CART-immunoreactive fibers and 96 +/- 2.8% NPY-immunoreactive neurons expressed cFos during fasting

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

14 choice, high-fat, high-sugar diet, intra-Acb NPY increased intake of fat, but not sugar or chow, and

15 Second, we measured the effect of intra-Acb NPY on neuronal activity using in vivo electrophysiology

16 Intra-Acb NPY reduced neuronal firing, as well as preproenkephalin

17 a support a role and mechanism for intra-Acb NPY-induced fat intake.

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

19 4 (DPP4)/CD26 by endothelial cells activates NPY-mediated signaling by increasing the bioavailability

20 Additionally, NPY and Y5R were upregulated in a BDNF-independent manne

21 rons, and the expression of tdTomato in AgRP-NPY neurons and tanycytes, were significantly decreased

22 e tdTomato-expressing cells were mainly AgRP-NPY neurons and tanycytes.

23 ptor-mediated responses in terminals of AgRP-NPY neurons onto two of their postsynaptic targets (Arc

24 ctional expression of P2X4 receptors on AgRP-NPY neuron somata, but instead, we found clear evidence

25 for FD-induced increases in feeding and AgRP/NPY.

26 ation non-specifically depolarizes both AgRP/NPY and POMC neurons but a strong inhibitory input to PO

27 l evidence that FD-induced increases in AgRP/NPY may be a direct PPARgamma-dependent process that con

28 trigger food hoarding/intake, increase AgRP/NPY, and possibly is necessary for FD-induced increases

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

30 creases in PPARgamma exclusively within AgRP/NPY neurons.

31 agouti-related protein/neuropeptide Y (AgRP/NPY)-expressing neurons but induces no net response in p

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

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

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

35 n polymerization pathway is triggered via an NPY motif (Y454).

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

37 oneally administered ROSI increases AgRP and NPY in ad libitum-fed animals; (4) whether intraperitone

38 2 prevented FD-induced increases in AgRP and NPY in both species.

39 ROSI increased AgRP and NPY similarly to FD, and GW9662 prevented FD-induced inc

40 nism blocks FD-induced increases in AgRP and NPY; and finally, (5) whether intraperitoneally administ

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

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

43 s a key mediator for postweaning feeding and NPY hyperphagia, and the PVH as one major downstream sit

44 asis for postweaning (nocturnal) feeding and NPY-mediated hyperphagia.

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

46 fasting-induced re-feeding, and insulin and NPY induced c-Fos induction in the same group of PVH neu

47 Reduced NPY and NPY receptor expression is associated with numerous neur

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

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

50 aling via ERK and Akt through the NPY R1 and NPY R2 receptors.

51 Numerous NPY(+) /somatostatin(+) and NPY(+) /somatostatin(-) fibers were observed, suggesting

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

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

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

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

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

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

58 In addition, arcuate NPY neurons exhibited abnormal electrophysiological resp

59 y, we could show that the impedimetric based NPY-receptor activation monitoring is not restricted to

60 ther, our novel impedance spectroscopy based NPY-receptor activation monitoring system offers the opp

61 haviors, underlying the interactions between NPY and CRF in the regulation of binge alcohol drinking

62 No colocalization was noted between NPY and TH or DbetaH immunoreactivities.

63 also reduced postweaning feeding and blunted NPY-induced hyperphagia.

64 raphic binding revealed the presence of both NPY and galanin receptors, while functional receptor bin

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

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

67 results revealed that PVH C-Fos induction by NPY is mediated by an indirect action, which is at least

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

69 rspective on extinction memory modulation by NPY, our findings suggest that elevated mPFC NPY in gene

70 system and can be activated specifically by NPY-8 in cell-based assays.

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

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

73 refed animals were immunostained with cFos, NPY, and CART antisera.

74 arization and perivascular fibers containing NPY.

75 ed by the expression of neuropeptide Y::Cre (NPY::Cre) act to gate mechanical itch.

76 Decreased NPY signaling in the Ce might contribute to the altered

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

78 rsed hyperphagia and obesity and reduced DMH NPY levels.

79 Mice in which dorsal NPY::Cre-derived neurons are selectively ablated or sile

80 Y1 BiFC homodimer had no impact on efficient NPY-stimulated endocytosis, demonstrating that single-si

81 y treatments based on viral vectors encoding NPY or galanin have been shown to effectively suppress s

82 Together these results identify endogenous NPY as a novel and potent inhibitory neuromodulator with

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

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

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

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

87 The almost equal NPY-cer bleaching when probed with TIR and epifluorescen

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

89 n different cell lines that natively express NPY-receptors and proof the specificity of the observed

90 we generated a lentiviral vector expressing NPY fused to a brain transport peptide (apoB) for widesp

91 FG(+) /NPY(+) cells were identified within the amygdalostriatal

92 Finally, NPY produced normal C-Fos induction in the PVH with disr

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

94 dies in human brain tissue, and advocate for NPY as a more appropriate candidate than galanin for fut

95 ional receptor binding was only detected for NPY, suggesting that galanin receptor signaling may be i

96 identify NPYR-1 as the cognate receptor for NPY-8, a neuropeptide required for sexual maturation and

97 These data demonstrate a clear role for NPY as a negative regulator of monocyte recruitment into

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

99 ly, selective deletion of Snord116 only from NPY expressing neurons mimics almost exactly the global

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

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

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

103 g autophagy, and also increases hypothalamic NPY levels, we hypothesized that NPY could have a releva

104 Modulation of hypothalamic NPY levels may be considered a potential strategy to pro

105 hown that, in aged animals, the hypothalamic NPY levels decrease.

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

107 howed a significant reduction (P < 0.001) in NPY-immunoreactivity in the IN.

108 We show that mice deficient in NPY have increased influx of monocytes into the brain an

109 ortex showed only a significant increase, in NPY neurons in supragranular layers (mean cells/mm(2) +/

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

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

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

113 als to a conditioned fear paradigm increased NPY gene expression within the AStr, whereas no changes

114 NMR measurements of specific isotope-labeled NPY in complex with in vitro folded Y2R reconstituted in

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

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

117 t of energy expenditure accompanied by lower NPY and increased POMC mRNA levels.

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

119 ing (mainly nocturnal) feeding and mediating NPY-induced hyperphagia.

120 NPY, our findings suggest that elevated mPFC NPY in gene polymorphism rs16147 carriers or after chron

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

122 anistically, in rodent hypothalamic neurons, NPY increases autophagy through the activation of NPY Y1

123 eased numbers of proopiomelanocortin but not NPY neurons and was accompanied by increased expression

124 ptide Y receptor 1 (NPY1R) and NPY5R but not NPY or NPY2R in the Ce predicted elevated AT; mRNA level

125 in neurons expressed Y1R and arcuate nucleus NPY neurons projected to the Acb.

126 Numerous NPY(+) /somatostatin(+) and NPY(+) /somatostatin(-) fibe

127 m channels as major reasons for the observed NPY-induced impedance increase.

128 unofluorescence revealed that 94 +/- 2.1% of NPY-immunoreactive neurons were contacted by CART-immuno

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

130 o NPY, likely contributing to the absence of NPY-induced phase advances of PER2::LUC rhythms in organ

131 site that mediates the orexigenic action of NPY.

132 The central actions of NPY and CRF have opposing functions in the regulation of

133 of experiments to investigate the actions of NPY in the Acb.

134 ncreases autophagy through the activation of NPY Y1 and Y5 receptors, and this effect is tightly asso

135 sults from the inhibition of the activity of NPY/AgRP/GABA neurons (NAG) in the arcuate nucleus of th

136 ood choice after bilateral administration of NPY in the Acb in rats on a free-choice diet of saturate

137 d clinical studies support an association of NPY with trauma-evoked syndromes such as posttraumatic s

138 study, we examined functional attributes of NPY in the infralimbic (IL) cortex, an area that regulat

139 Blockade of NPY Y1 receptors was sufficient to generate spike and wa

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

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

142 vated monocytes were increased in the CNS of NPY(-/-) mice following virus infection, suggesting that

143 r (PTSD), although the exact contribution of NPY is not clear.

144 Contribution of NPY to PTSD symptomology is unclear.

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

146 assessed in rats by examining the degree of NPY coexpression within interneurons or catecholaminergi

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

148 Overall, increased delivery of NPY to the CNS for AD might be an effective therapy espe

149 alin and dynorphin neurons and the effect of NPY on preproenkephalin messenger RNA levels in the stri

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

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

152 The objective was to examine the effects of NPY variant rs16147 on central obesity and abdominal fat

153 he neuroprotective and neurogenic effects of NPY-apoB appeared to involve signaling via ERK and Akt t

154 ween the molecular and behavioral effects of NPY.

155 Furthermore, pharmacological elevation of NPY prevented bone marrow impairments in a mouse model o

156 This suggests that enhancement of NPY signaling might reduce the risk to develop psychopat

157 Expression of NPY and its receptors was evaluated in corresponding sam

158 In human NB tissues, the expression of NPY and Y5R positively correlated with the expression of

159 discordance with the abundant expression of NPY receptors, a group of inhibitory Gi protein coupled

160 the bioavailability of the truncated form of NPY.

161 ts were not commonly observed upon fusion of NPY-cer-containing granules.

162 The C-terminal alpha-helix of NPY, which is formed in a membrane environment in the ab

163 Although the importance of NPY's actions in the BLA is well documented, little is k

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

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

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

167 effects were blocked by prior inhibition of NPY Y1 or Y5 receptors.

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

169 sely stained, along with increased levels of NPY, suggesting profound alteration of the PLCbeta2/IP3

170 ased system for the activation monitoring of NPY-receptors in living cells.

171 -anaesthetized female rats, nanoinjection of NPY into the paraventricular nucleus of the hypothalamus

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

173 Conversely, the total numbers of NPY- and VIP-immunoreactive neurons were reduced by 55%

174 y was used to identify the precise origin of NPY projections to the BLA.

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

176 rved, suggesting at least two populations of NPY fibers within the BLA.

177 nto IL projection neurons in the presence of NPY.

178 he nervous system, through the production of NPY, can suppress monocyte trafficking to the brain and

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

180 To determine whether replacement of NPY could ameliorate some of the neurodegenerative and b

181 They also reveal a new role of NPY as a regulator of the bone marrow microenvironment a

182 of this study was to investigate the role of NPY on autophagy in the hypothalamus.

183 However, little is known about the role of NPY variations in diet-induced change in adiposity.

184 nted, little is known about the source(s) of NPY fibers to this region.

185 The current studies identified sources of NPY projections to the BLA by using a combination of ana

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 The subpopulation of NPY neurons in the AStr also coexpressed somatostatin.

189 n NB cells, BDNF stimulates the synthesis of NPY and induces expression of another one of its recepto

190 expression of Y2R on monocytes, treatment of NPY(-/-) mice with a truncated, Y2R-specific NPY peptide

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

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

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

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

195 onal in vitro models and mice overexpressing NPY in the hypothalamus, we observed that NPY stimulates

196 emical correlate of arousal, and potentiates NPY's inhibition of SCN Per1-EGFP cells.

197 ve been reported to have elevated prefrontal NPY expression.

198 f relevance to PTSD, elevation of prefrontal NPY attributable to the genetic polymorphism rs16147 may

199 ns associated with stress circuits providing NPY input to the BLA and demonstrated that a unique NPY

200 Collectively, these data suggest that PVN NPY inputs converge with alpha-MSH to influence presympa

201 by agonist/antagonist studies in recombinant NPY-receptor expressing cell lines.

202 The recombinant NPY-apoB effectively reversed neurodegenerative patholog

203 human lung airway explants with recombinant NPY increased airway contractility.

204 Reduced NPY and NPY receptor expression is associated with numer

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

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

207 Elevated serum NPY levels correlated with an adverse clinical presentat

208 emic NPY and NB progression identifies serum NPY as a novel NB biomarker.

209 NPY(-/-) mice with a truncated, Y2R-specific NPY peptide suppressed the incidence of retrovirus-induc

210 BAergic interneurons, including the striatal NPY-neurogliaform interneuron.

211 The correlation between elevated systemic NPY and NB progression identifies serum NPY as a novel N

212 By demonstrating that NPY release modulates hippocampal synaptic plasticity an

213 We determined that NPY promotes AHR through the induction of Rho kinase act

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

215 We found that NPY Y1 receptor (Y1R) activation in the BNST suppressed

216 ypothalamic NPY levels, we hypothesized that NPY could have a relevant role on autophagy modulation i

217 These results indicate that NPY promotes neuroprotection and restores bone marrow dy

218 with TIR and epifluorescence indicated that NPY-cer equilibrated within the 300 ms bleach pulse, and

219 ng NPY in the hypothalamus, we observed that NPY stimulates autophagy in the hypothalamus.

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

221 Here we show that NPY-deficient mice have significantly reduced hematopoie

222 e following virus infection, suggesting that NPY suppresses the infiltration of both cell types.

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

224 The NPY receptors known as Y receptors are classified into t

225 The NPY Y1 receptor antagonist BIBO3304 completely abolished

226 non of relevance in drug research beyond the NPY receptor field.

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

228 gical conditions may be mainly driven by the NPY-positive inhibitory neurons.

229 the first time to quantitatively detect the NPY-receptor activation directly without a secondary or

230 Further, the NPY-Y1 pathway may offer a potential therapeutic target

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

232 Furthermore, we could monitor the NPY-receptor activation in different cell lines that nat

233 ating monocytes expressed high levels of the NPY receptor Y2R.

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

235 Expression of the NPY Y1 receptor (Y1R) is highly concentrated in the nucl

236 In summary, the NPY/Y5R axis is an inducible survival pathway activated

237 Our data indicate that the NPY rs16147 genotypes affect the change in abdominal adi

238 Therefore, the NPY/Y5R pathway may become a novel therapeutic target fo

239 nvolve signaling via ERK and Akt through the NPY R1 and NPY R2 receptors.

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

241 caused depression of the maximal response to NPY (calcium assay) by up to 90% in a concentration- and

242 nificantly fewer silent cells in response to NPY, likely contributing to the absence of NPY-induced p

243 owth, and disrupted hyperphagic responses to NPY.

244 Similar to NPY-8, knockdown of this receptor results in loss of dif

245 hat was restored by treatment with truncated NPY.

246 Analogues of the argininamide-type NPY Y1 receptor (Y1R) antagonist BIBP3226, bearing carba

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

248 n used extensively to examine the underlying NPY orexigenic neural pathways.

249 ut to the BLA and demonstrated that a unique NPY projection from the AStr may participate in the regu

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

251 sing retrograde tracing, we examined whether NPY neurons in the arcuate nucleus projected to the Acb.

252 To test whether NPY and galanin have antiepileptic actions in human epil

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

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

255 el of chemotherapy-induced SNS injury, while NPY injection into conditional knockout mice lacking the

256 h, Taeniopygia guttata, its interaction with NPY, and their response to dynamic energy states.

257 glutamate receptors-2 mGlu2, neuropeptide-Y NPY, and mineralocorticoid receptors MR).

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

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

260 Bioconjugates containing the neuropeptide Y (NPY) analogue [F(7),P(34)]-NPY as targeting moiety are a

261 ission in neurons expressing neuropeptide Y (NPY) and agouti-related peptide (AgRP) via GABA-dependen

262 stress and reward, including neuropeptide Y (NPY) and corticotropin-releasing factor (CRF).

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

264 r of interneurons expressing neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP), and th

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

266 model of the peptide hormone neuropeptide Y (NPY) bound to its human G-protein-coupled Y2 receptor (Y

267 al amygdaloid complex (BLA), neuropeptide Y (NPY) buffers against protracted anxiety and fear.

268 CA1 interneurons expressing neuropeptide Y (NPY) contributes prominently to this dynamic filter by i

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

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

271 owever, the specific role of neuropeptide Y (NPY) in this process has not been systematically studied

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

273 Neuropeptide Y (NPY) is a hypothalamic neuropeptide that plays a promine

274 Neuropeptide Y (NPY) is a well-established orexigenic peptide and hypoth

275 Neuropeptide Y (NPY) is one of the major neuropeptides present in the hy

276 Neuropeptide Y (NPY) is one of the most abundant protein transmitters in

277 ons that fluorescent-labeled neuropeptide Y (NPY) is usually released within 200 ms after fusion, whe

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

279 current study, we found that neuropeptide Y (NPY) suppressed monocyte recruitment to the CNS in a mou

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

281 BiFC system to study example neuropeptide Y (NPY) Y1 receptor dimers.

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

283 Neuropeptide Y (NPY), a brain neuromodulator that has been strongly impl

284 Neuropeptide Y (NPY), a stress modulatory transmitter, is associated wit

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

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

287 py-induced cell death, while neuropeptide Y (NPY), acting via its Y2 receptor (Y2R), is an autocrine

288 proopiomelanocortin (POMC), neuropeptide Y (NPY), agouti-related peptide (AGRP), somatostatin, and d

289 els of hypothalamic GHS-R1a, neuropeptide Y (NPY), and agouti-related protein (AgRP), suggesting that

290 in (PV), calretinin (CR) and neuropeptide Y (NPY), and somatostatin (SOM) and glial fibrillary acidic

291 N clock-resetting effects of neuropeptide Y (NPY), another neurochemical correlate of arousal, and po

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

293 rin-releasing peptide (GRP), neuropeptide Y (NPY), nitric oxide synthase (NOS), serotonin, substance

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

295 athway modulating release of neuropeptide Y (NPY), which stimulates OE stem cell activity.

296 er cholecystokinin (CCK)- or neuropeptide Y (NPY)-expressing interneurons.

297 be precipitated by a loss of neuropeptide Y (NPY)-mediated local circuit inhibition and a subsequent

298 uncates the neurotransmitter neuropeptide Y (NPY).

299 rates of fluorescent-tagged neuropeptide-Y (NPY) (within 200 ms) and tissue plasminogen activator (t

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