ライフサイエンスコーパス: PACAP

1 PACAP enhanced, however, excitatory synaptic transmissio

2 PACAP has also been shown to induce neurite outgrowth in

3 PACAP is a peptide with neuroprotective activity, which

4 PACAP is highly expressed in the amygdala, a subcortical

5 PACAP is involved in certain adult behaviors.

6 PACAP is upregulated in DRG neurons as a result of injur

7 PACAP levels and ADCYAP1R1 SNPs may serve as useful biom

8 PACAP not only stimulated prosurvival ERK1/2 and ERK5 ac

9 PACAP or microglia antagonists (50 nl) (PACAP(6-38), 15

10 PACAP receptor (PACR1) stimulation triggered both G(i)al

11 PACAP signaling to neuritogenesis was also impaired by d

12 PACAP stimulated both c-Rel and p52 NF-kappaB subunit ge

13 PACAP stimulation did not evoke action potential firing

14 PACAP(6-38) caused a 161% increase, whereas minocycline

15 PACAP-38 activation of all downstream targets of cAMP wa

16 PACAP-containing cell groups were found to be retrograde

17 PACAP-induced c-Rel nuclear translocation was inhibited

18 PACAP-induced potentiation of glutamatergic synaptic res

19 PACAP-treated rats ate smaller meals of normal duration,

20 To test for a PACAP/Hh interaction in the initiation or propagation of

21 propagation of these tumors, we introduced a PACAP mutation into ptc1 mutant mice.

22 AC1 receptor antagonist (experiment 2), or a PACAP agonist (experiment 3) without footshock.

23 p receptor using short-hairpin RNA abolished PACAP mitogenic stimulation at E10.5.

24 Accordingly, PACAP stimulation resulted in TrkA-dependent phosphoryla

25 n NG108-15 cells reconstituted high affinity PACAP binding and PACAP-dependent cAMP generation but wi

26 PAC1 receptors, reconstituted high affinity PACAP binding and PACAP-dependent elevation of both cAMP

27 ing PACAP in stress biology, and how altered PACAP expression and signaling may result in psychopatho

28 Although PACAP increased excitability in 90% of guinea pig cardia

29 tra-CeA (but not intra-basolateral amygdala) PACAP dose-dependently induced anorexia and body weight

30 treatment with forskolin, cAMP analogs, and PACAP were measured in Neuroscreen-1 (NS-1) cells, a PC1

31 co-expression of the neuropeptides BDNF and PACAP.

32 econstituted high affinity PACAP binding and PACAP-dependent cAMP generation but without a correspond

33 econstituted high affinity PACAP binding and PACAP-dependent elevation of both cAMP and intracellular

34 In isolated islets, carbachol and PACAP/VIP synergistically promote beta-cell proliferatio

35 d three A10-elevated peptides (GRP, CGRP and PACAP) were further examined in both alpha-synuclein ove

36 l projections containing colocalized CtB and PACAP immunostaining were identified in the SCN, the lat

37 iple labeling immunofluorescence for CTb and PACAP.

38 fficking did not blunt the PACAP effect, and PACAP/PAC1R signaling still increased neuronal cAMP prod

39 hen short expression was 15-fold greater and PACAP inhibited mitogenesis.

40 ic neurons, both Homer 1a overexpression and PACAP treatment reversed the decrease in mGluR1-mediated

41 e and function between C57BL/6 wild-type and PACAP-/- male mice, at 4 and 15 months of age.

42 pecific roles (if any) of endogenous VIP and PACAP in the protection against autoimmune diseases have

43 Intrathecal infusion of the PACAP antagonist PACAP(6-38) or the microglia antagonists minocycline and

44 solution structure of the potent antagonist PACAP (residues 6'-38') complexed to the N-terminal extr

45 infusions with the PACAP receptor antagonist PACAP(6-38) blocked chronic constriction injury-induced

46 BNST infusions of the PAC1/VPAC2 antagonist, PACAP 6-38, prevented footshock-induced reinstatement of

47 ockdown of the receptor effectors attenuated PACAP-mediated Akt activation.

48 signal-regulated kinase signaling attenuated PACAP-induced CeA neuronal activation and nociceptive re

49 In hippocampal autapses, PACAP treatment uncoupled postsynaptic mGluR5 from EPSC

50 as a systematic correlation analysis between PACAP level, cognitive performance, and pathologic sever

51 conducted to clarify the association between PACAP biomarkers and preclinical, mild cognitive impairm

52 natomical foundation for interaction between PACAP and its potential target neurons in the PVN, such

53 targeting one of these genes, Egr1, blocked PACAP-induced neuritogenesis, and siRNA targeting anothe

54 3-kinase gamma-selective inhibitors blocked PACAP-stimulated Akt phosphorylation in primary neuronal

55 Neither siRNA blocked PACAP's PKA-dependent antiproliferative effects.

56 administration elevated BNST PACAP, and BNST PACAP receptor activation was necessary and sufficient f

57 s cognate PAC1 receptor transcript, and BNST PACAP signaling may mediate the maladaptive changes asso

58 Cocaine self-administration elevated BNST PACAP, and BNST PACAP receptor activation was necessary

59 water intake and weight loss following BNST PACAP infusion.

60 , cocaine self-administration increased BNST PACAP transcript levels similar to what we have previous

61 costerone levels 30 min following intra-BNST PACAP infusion in male rats that had been previously exp

62 In experiment 3, intra-BNST PACAP infusion reinstated previously extinguished cocain

63 cuits underlying the responses to intra-BNST PACAP, and may result in different anxiety-like response

64 or endocrine response to a subthreshold BNST PACAP infusion.

65 These data suggest that BNST PACAP systems may be viable targets for relapse preventi

66 minant-negative Rap1 expression impairs both PACAP-induced neuritogenesis and Egr1 activation by PACA

67 ion event was identified as critical to both PACAP-mediated transactivation and TrkA-dependent Rit ac

68 ng that cAMP elevation and ERK activation by PACAP are linked through Rap1.

69 nduced neuritogenesis and Egr1 activation by PACAP, suggesting that cAMP elevation and ERK activation

70 ponent of the cell size increase elicited by PACAP.

71 neuronal excitability was only increased by PACAP.

72 CREB phosphorylation induced by PACAP was blocked by H-89.

73 harmacological profile of their induction by PACAP (i.e., mimicking that of neuritogenesis).

74 cause proarrhythmogenic changes mediated by PACAP and microglia.

75 echanisms mediating the anorexia produced by PACAP in the central nucleus of the amygdala (CeA), a li

76 interaction, and attention were produced by PACAP, as reflected by increases in reward thresholds, d

77 hway in neuronal differentiation promoted by PACAP.

78 The liver protection rendered by PACAP peptides was accompanied by diminished neutrophil/

79 er, potentiation of synaptic transmission by PACAP was dependent on postsynaptic activation of protei

80 Intra-CeA PACAP-induced anorexia was blocked by coinfusion of eith

81 n the central nucleus of the amygdala [CeA]) PACAP immunoreactivity, extracellular signal-regulated k

82 corroborate growing data implicating central PACAP activation in mediating the consequences of stress

83 ght loss, and both the activation of central PACAP systems as well as neuronal activity in the BNST h

84 Furthermore, CGRP, PACAP, and VIP suppress phosphorylation of IkappaB kinas

85 gest that the inhibitory activities of CGRP, PACAP, and VIP on LC function are mediated, at least in

86 In conclusion, PACAP-immunoreactive projections with colocalized CtB re

87 ve intestinal peptide and also differentiate PACAP residues involved in binding to the N-terminal ext

88 e coupling to adenylate cyclase and to drive PACAP-dependent differentiation but do not express PAC1

89 To elucidate PACAP interactions, a compendium of microarrays represen

90 These results demonstrate that endogenous PACAP provides protection in EAE and identify PACAP as a

91 se enzymes or endocytosis to block endosomal PACAP receptor extracellular signal-regulated kinase sig

92 = 5-8 per group per experiment) to evaluate PACAP plasticity and signaling in nociceptive and stress

93 Exogenous PACAP and substance P initiated a slow depolarization in

94 In rodents, exogenous PACAP administration can produce persistent elevations i

95 ide evidence that stimulation with exogenous PACAP and native neuronal stress stimulation both lead t

96 CGRP positive neurons expressed PACAP but not glutamate.

97 dependent signaling pathway and required for PACAP-dependent cAMP response element-binding protein ac

98 on of two genes, Egr1 and Vil2, required for PACAP-dependent neuritogenesis and increased cell size,

99 DNA repair function of APE1 was required for PACAP-mediated neuroprotection.

100 nate and learned fear, suggesting a role for PACAP-mediated signaling in fear-related behaviors.

101 uctural basis for hPAC1-R(S) selectivity for PACAP versus the vasoactive intestinal peptide and also

102 Tumors from PACAP/ptc1 mutant mice retained PACAP receptor gene expr

103 We investigated the roles of glutamate, PACAP, and microglia on RVLM catecholaminergic neurons d

104 It remains unknown, however, whether and how PACAP affects neuronal and synaptic functions in the amy

105 ACAP provides protection in EAE and identify PACAP as an intrinsic regulator of Treg abundance after

106 ing male Sprague Dawley rats, we examined if PACAP (.25-1.0 microg, intracerebroventricular infusion)

107 Finally, we examined if PACAP affects performance in the 5-choice serial reactio

108 We also examined if PACAP alters interactions with a conspecific in the soci

109 the PACAPergic systems, the data implicating PACAP in stress biology, and how altered PACAP expressio

110 We include our work implicating PACAP signaling within the bed nucleus of the stria term

111 nes the exclusive requirement for this AC in PACAP signaling, but that the coupling of the cAMP senso

112 r structure was remarkably well conserved in PACAP-/- animals.

113 However, we now find that mice deficient in PACAP exhibited a decrease in the BrdU labeling index (L

114 Deficits in PACAP are associated with clinical severity in the MCI a

115 lts show that testicular aging is delayed in PACAP-/- animals.

116 the hepatocellular damage was exacerbated in PACAP-deficient mice.

117 ain, has been hypothesized to be involved in PACAP effects, but the reports are conflicting so far.

118 that induces apoptosis, is down-regulated in PACAP-/- animals.

119 show that chronic neuropathic pain increases PACAP expression at multiple tiers along the spinoparabr

120 Our data suggest that chronic pain-induced PACAP neuroplasticity and signaling in spinoparabrachioa

121 suggesting that the effects of BNST-infused PACAP were not mediated by leakage into the ventricular

122 id receptor agonist, SNC 80, did not inhibit PACAP-induced neurogenesis even though it did reduce CRE

123 nctional Trk receptors, was found to inhibit PACAP-mediated Rit activation, whereas constitutively ac

124 We found that intracerebroventricular PACAP treatment induced anxiety-like behavior in the ele

125 However, intrathecal PACAP did not show additive effects, suggesting that the

126 In intrathecal PACAP-antagonist-treated rats, both BP and HR increased,

127 eadily triggered the expression of intrinsic PACAP and its receptors, whereas the hepatocellular dama

128 ion by the G protein-coupled receptor ligand PACAP (pituitary adenylyl cyclase-activating peptide).

129 We measured PACAP and its receptor (PAC1) levels using enzyme-linked

130 Forskolin and dibutyryl cAMP mimic PACAP's neuritogenic and cell morphological effects, sug

131 Minor PACAP projections with scattered double-labeled neurons

132 Moreover, PACAP inhibited proliferation of cell lines derived from

133 Moreover, PACAP-evoked secretion was sensitive to block by nickel

134 tify an unsuspected role for Rin in neuronal PACAP signaling and establish a novel Galpha-Src-Rin-HSP

135 ion in ipRGCs and output by the neuropeptide PACAP, which provide stable pupil maintenance across the

136 NGF, PACAP, and a combination of the two stimulated both intr

137 PACAP or microglia antagonists (50 nl) (PACAP(6-38), 15 pmol; minocycline 10 mg/ml) microinjecte

138 the increase in excitability caused by 1 nM PACAP so that only 4 of 13 neurones exhibited a tonic fi

139 After addition of 1 nM PACAP to the bath, 7 of 9 neurones exhibited a tonic fir

140 The ability of PACAP-38 and forskolin to activate three cAMP sensors do

141 lated with sustained pro-mitogenic action of PACAP beyond the developmental switch.

142 The actions of PACAP or microglia on RVLM neurons do not cause sympatho

143 nt studies have shown that administration of PACAP, like VIP, can attenuate dramatically the clinical

144 n rat brain slices, exogenous application of PACAP did not affect either resting membrane potential o

145 ized subjects, a sex-specific association of PACAP blood levels with fear physiology, PTSD diagnosis

146 s resulted in acquisition by PC12-G cells of PACAP-dependent [Ca2+]i increase and extracellular Ca2+

147 A comparison of PACAP and PAC1 levels among the healthy controls, MCI-AD

148 Deletion of a single copy of PACAP increased MB incidence approximate 2.5-fold, to 66

149 PTSD and are known to have high densities of PACAP receptors.

150 g protein 1 (RAMP1), and the distribution of PACAP and glutamate in rhesus and rat TG.

151 he BNST with a normally subthreshold dose of PACAP.

152 n of anorexia is a well-documented effect of PACAP, the central sites underlying this phenomenon are

153 contrast to the potent and rapid effects of PACAP in ERK1/2 phosphorylation, PACAP stimulated Akt ph

154 her characterizing the behavioral effects of PACAP in rats and at determining the role of central CRF

155 receptors might mediate synaptic effects of PACAP in the CeL.

156 The suppressive effects of PACAP was as effective as dexamethasone in all of their

157 sor exposure may depend on the expression of PACAP in the bed nucleus of the stria terminalis (BNST).

158 Expression of PACAP receptors in neuroendocrine rather than nonneuroen

159 MOG immunization of PACAP-deficient mice triggered heightened clinical and p

160 ur novel findings document the importance of PACAP-mediated cAMP-PKA signaling in hepatic homeostasis

161 ral stages to determine transcript levels of PACAP and corresponding receptors.

162 Nevertheless, the exact localization of PACAP-producing neurons that project to the PVN is not u

163 issue slices to investigate the mechanism of PACAP-evoked calcium entry.

164 ey brain, we characterized the occurrence of PACAP in melanopsin-expressing ipRGCs and in the retinal

165 observations indicate a multisite origin of PACAP innervation to the PVN and provide a strong chemic

166 The partitioning of PACAP-mediated Akt signaling in endosomes may be a key m

167 The expression pattern of PACAP and glutamate suggests a possible interaction betw

168 thylxanthine (IBMX) increased the potency of PACAP at inducing neurite outgrowth by ten-fold.

169 al studies are needed to clarify the role of PACAP deficits in the predisposition to, pathogenesis of

170 ptically, consistent with the known roles of PACAP in control of fear-related behaviors.

171 aimed at characterizing the transcriptome of PACAP-differentiated PC12 cells revealed an increase in

172 tic responses persisted after the washout of PACAP and was blocked by the VPAC1 receptor antagonist,

173 We show that, in 4-month-old PACAP-/- mice, steroidogenesis (evaluated by levels of t

174 stingly, the CRF antagonist had no effect on PACAP-induced increased plasma corticosterone, reduction

175 rin mimicked the effects of AC6 silencing on PACAP signaling, without attenuating forskolin signaling

176 ells to either forskolin, dibutyryl cAMP, or PACAP revealed a small group of cAMP-dependent target ge

177 PKA- and Epac-independent signaling pathway: PACAP --> adenylate cyclase --> cAMP --> ERK --> neurito

178 Between ERK and Akt pathways, PACAP-stimulated Akt signaling was the primary cascade t

179 The neurotrophic peptide PACAP (pituitary adenylate cyclase-activating polypeptid

180 uitary adenylate cyclase-activating peptide (PACAP) and their class II G protein-coupled receptors VP

181 uitary Adenylate Cyclase Activating Peptide (PACAP) impacts levels of cyclic AMP, a key second messen

182 uitary adenylate cyclase-activating peptide (PACAP) is an excitatory neuroactive peptide transmitter

183 uitary adenylate cyclase-activating peptide (PACAP) systems in several psychiatric disorders associat

184 uitary adenylate cyclase-activating peptide (PACAP) systems in the bed nucleus of the stria terminali

185 uitary adenylate cyclase activating peptide (PACAP) to induce native Homer 1a expression.

186 uitary adenylate cyclase-activating peptide (PACAP) which contributed to the generation of a local pr

187 uitary adenylate cyclase-activating peptide (PACAP), a cAMP-activating agent, is highly expressed in

188 uitary adenylate cyclase-activating peptide (PACAP), a polypeptide that regulates testicular steroido

189 tuitary adenylyl cyclase-activating peptide (PACAP), which has been shown to regulate cerebellar gran

190 adenylate cyclase (PAC) activating peptide (PACAP)/PAC1 to affect ERK/MAPK, and in the early night,

191 effects of PACAP in ERK1/2 phosphorylation, PACAP stimulated Akt phosphorylation in a late phase of

192 ry adenylate cyclase-activating polypeptide (PACAP) activates each.

193 ry adenylate cyclase-activating polypeptide (PACAP) and glutamate were examined and related to the CG

194 ry adenylate cyclase activating polypeptide (PACAP) and its cognate PAC1 receptor transcript, and BNS

195 ry adenylate cyclase-activating polypeptide (PACAP) and its receptor PAC1 have been proposed to have

196 ry adenylate cyclase-activating polypeptide (PACAP) associated with posttraumatic stress disorder (PT

197 ry adenylate cyclase-activating polypeptide (PACAP) axons.

198 ry adenylate cyclase-activating polypeptide (PACAP) binding to specific PAC(1) receptor isoforms can

199 ry adenylate cyclase activating polypeptide (PACAP) has critical roles in central neurocircuits media

200 ry adenylate cyclase-activating polypeptide (PACAP) in patients with neuropathologically confirmed Al

201 ry adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide with autocrine and paracrine ne

202 ry adenylate cyclase-activating polypeptide (PACAP) is a pleiotropic neuropeptide expressed in the br

203 ry adenylate cyclase-activating polypeptide (PACAP) is a potent neuropeptide that possesses both neur

204 ry adenylate cyclase-activating polypeptide (PACAP) is a trophic factor that promotes neuronal surviv

205 ary adenylyl cyclase-activating polypeptide (PACAP) is a widely expressed neuropeptide originally dis

206 ry adenylate cyclase activating polypeptide (PACAP) is an excitatory neuropeptide with neuroprotectiv

207 ry adenylate cyclase-activating polypeptide (PACAP) is known to broadly regulate the cellular stress

208 ry adenylate cyclase-activating polypeptide (PACAP) or substance P released during tetanic neural sti

209 ry adenylate cyclase-activating polypeptide (PACAP) plays an important role in regulating stress effe

210 ry adenylate cyclase-activating polypeptide (PACAP) receptor is a class II G protein-coupled receptor

211 ry adenylate cyclase-activating polypeptide (PACAP), a member of the secretin-glucagon-VIP family, ha

212 ry adenylate cyclase-activating polypeptide (PACAP), an endogenously occurring small neuropeptide, in

213 ry adenylate cyclase-activating polypeptide (PACAP), and vasoactive intestinal peptide (VIP) suppress

214 ry adenylate cyclase-activating polypeptide (PACAP)-38, or the diterpene forskolin as an AC-proximal

215 ry adenylate cyclase-activating polypeptide (PACAP).

216 ry adenylate cyclase-activating polypeptide (PACAP).

217 ry adenylate cyclase-activating polypeptide (PACAP)/PAC1 receptor system represents one of the main r

218 ry adenylate cyclase-activating polypeptide (PACAP, also known as ADCYAP1).

219 ry adenylate cyclase-activating polypeptide (PACAP; Adcyap1) and its cognate PAC1 receptor (Adcyap1r1

220 ry adenylate cyclase activating polypeptide (PACAP; Adcyap1) is a potent neurotransmitter/neurotrophi

221 ry adenylate cyclase-activating polypeptide (PACAP; ADCYAP1) may contribute to proliferation control

222 y adenylate cyclase-activating polypeptides (PACAP) in a murine model of partial liver "warm" ischemi

223 tuitary adenylyl cyclase-activating protein (PACAP), another PNMT transcriptional activator, cooperat

224 fficient levels of PAC1 receptors to provide PACAP-saturable coupling to adenylate cyclase and to dri

225 ored liver damage in otherwise IR-resistant, PACAP-conditioned mice.

226 Tumors from PACAP/ptc1 mutant mice retained PACAP receptor gene expression, and exhibited superinduc

227 In the retina, PACAP and melanopsin were found to be costored in 99% of

228 contribution of various brain areas sending PACAP innervation to the rat PVN by using iontophoretic

229 Here, we subjected PACAP-deficient mice to myelin oligodendrocyte glycoprot

230 ronal and endocrine cells and do not support PACAP-mediated neurosecretion.

231 summary, therapeutic interventions targeting PACAP and microglia could be a promising strategy for pr

232 the PACAP system promotes anorexia and that PACAP preferentially lessens the maintenance of feeding

233 system, the current studies demonstrate that PACAP activation of PAC(1)HOP1 receptors engages both MA

234 We also demonstrate that PACAP in the CeA exerts its anorectic effects via local

235 Our results demonstrate that PACAP/PAC1R complex endocytosis is a key step for the PA

236 2.5-fold, to 66%, thereby demonstrating that PACAP exerts a powerful inhibitory action on the inducti

237 While it is well established that PACAP mediates both neurotrophic and neurodevelopmental

238 The results provide genetic evidence that PACAP acts as a physiological factor that regulates the

239 At this stage, we found that PACAP evoked intracellular calcium fluxes and increased

240 Finally, we found that PACAP increased CRF levels in the paraventricular nucleu

241 Previously, we found that PACAP was an anti-mitogenic signal from embryonic day 13

242 Our findings support the idea that PACAP and its action on microglia at the level of the sp

243 These findings indicate that PACAP can be released by tetanic neural stimulation in v

244 Our results strengthen the notion that PACAP is a strong mediator of the behavioral response to

245 ler meals of normal duration, revealing that PACAP slowed feeding within meals by decreasing the regu

246 We further show that PACAP markedly reduces oxidative DNA stress and hippocam

247 Taken together, our data show that PACAP promotes both survival and neuritogenesis in PC12

248 Here, we show that PACAP-mediated Rit activation involves Src family kinase

249 We first showed that PACAP-driven survival and neuritic extension in PC12 cel

250 Our findings suggest that PACAP affects numerous domains often dysregulated in moo

251 These observations suggest that PACAP elicits temporally specific effects on cortical pr

252 These data suggest that PACAP receptor activation in posterior BNST subregions c

253 tional observations have also suggested that PACAP may be an excitatory neuropeptide at the level of

254 These observations suggested that PACAP released from preganglionic nerve terminals during

255 lts are consistent with data suggesting that PACAP dysregulation is associated with posttraumatic str

256 describe more recent studies suggesting that PACAP in the central nucleus of the amygdala may impact

257 g index (LI) in E9.5 cortex, suggesting that PACAP normally promotes proliferation at this stage.

258 The PACAP in the primary visual cortex did not correlate wit

259 The PACAP in the superior frontal gyrus and middle temporal

260 The PACAP levels in cerebrospinal fluid correlated with the

261 The PACAP levels in cerebrospinal fluid, the superior fronta

262 The PACAP peptide adopts a helical conformation when bound t

263 Subsequent addition of inhibitor after the PACAP-induced increase in excitability developed gradual

264 ibitor and immunoprecipitation analyses, the PACAP/PAC(1)HOP1 receptor-mediated Akt responses did not

265 Golgi vesicle trafficking did not blunt the PACAP effect, and PACAP/PAC1R signaling still increased

266 1R complex endocytosis is a key step for the PACAP modulation of cardiac neuron excitability.

267 In contrast, it is unclear if the PACAP-PAC1 receptor pathway has a role in human psycholo

268 ore, a single nucleotide polymorphism in the PACAP receptor gene ADCYAP1R1, adenylate cyclase activat

269 These data suggest that perturbations in the PACAP-PAC1 pathway are involved in abnormal stress respo

270 Likewise, the PACAP-induced increase in excitability was markedly decr

271 Intrathecal infusion of the PACAP antagonist PACAP(6-38) or the microglia antagonist

272 exchange factor (GEF), and the nature of the PACAP regulatory cascade remained unclear.

273 The pharmacodynamic model of the PACAP-PAC1 interaction best predicted cognitive function

274 rol RNA interference treatment prevented the PACAP effect, suggesting that it resulted specifically f

275 nucleotide polymorphisms (SNPs) spanning the PACAP (encoded by ADCYAP1) and PAC1 (encoded by ADCYAP1R

276 d dynamin I/II, respectively, suppressed the PACAP effect.

277 The findings indicate that the PACAP system modulates medial temporal lobe function in

278 Thus, the PACAP pathway provides for an important mechanism underl

279 is one of the brain areas through which the PACAP system promotes anorexia and that PACAP preferenti

280 Acute CeA infusions with the PACAP receptor antagonist PACAP(6-38) blocked chronic co

281 Thus, PACAP may upregulate excitatory neurotransmission in the

282 Thus, PACAP-38 potently stimulated two distinct and independen

283 y TrkA-Rit signaling as a key contributor to PACAP-dependent neuronal differentiation.

284 Clusters among genes directly linked to PACAP, and probable interactions between corresponding p

285 In contrast a peptide related to PACAP, vasoactive intestinal peptide (VIP) failed to ind

286 e adenylate cyclase isoform most relevant to PACAP's action.

287 Ca2+ influx-dependent manner in response to PACAP.

288 odel for understanding mechanisms underlying PACAP differentiation and neurogenesis.

289 modulator has ever been reported for the VIP/PACAP receptors, and there is a lack of specific VPAC(2)

290 In vitro, PACAP treatment not only diminished macrophage tumor nec

291 We hypothesize that in vivo PACAP released during preganglionic firing may modulate

292 division of the central nucleus (CeL), where PACAP-positive presynaptic terminals were predominantly

293 Here we ask whether PACAP is also involved in producing reinstatement in a m

294 We sought to determine whether PACAP and microglia mitigate the adverse effects of seiz

295 To evaluate whether PACAP-immunoreactive retinal projections are useful as a

296 We investigated whether PACAP causes acute or persistent alterations in behavior

297 dition, we identified the mechanism by which PACAP exerts its anxiogenic and pro-depressant effects,

298 ra toxin subunit B (CtB) in combination with PACAP staining.

299 gher number of apoptotic cells compared with PACAP-/- mice.

300 Male rats were microinfused with PACAP (0-1 mug per rat) into the CeA and home-cage food