ライフサイエンスコーパス: PACAP

1 PACAP enhanced, however, excitatory synaptic transmissio

2 PACAP is highly expressed in the amygdala, a subcortical

3 PACAP is involved in certain adult behaviors.

4 PACAP levels and ADCYAP1R1 SNPs may serve as useful biom

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

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

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

8 PACAP signaling to neuritogenesis was also impaired by d

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

10 PACAP stimulation did not evoke action potential firing

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

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

13 PACAP-induced c-Rel nuclear translocation was inhibited

14 PACAP-induced potentiation of glutamatergic synaptic res

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

16 GAD diagnosis overall (p = 0.19, g = 0.25), PACAP may be associated with GAD in females (p = 0.04, g

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

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

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

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

21 Accordingly, PACAP stimulation resulted in TrkA-dependent phosphoryla

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

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

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

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

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

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

28 co-expression of the neuropeptides BDNF and PACAP.

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

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

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

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

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

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

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

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

37 ecific microinfusion of the PAC1R antagonist PACAP(6-38) into the BNST dose-dependently blocked exces

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

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

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

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

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

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

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

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

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

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

48 3-kinase gamma-selective inhibitors blocked PACAP-stimulated Akt phosphorylation in primary neuronal

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

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

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

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

53 water intake and weight loss following BNST PACAP infusion.

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

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

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

57 Intra-BNST PACAP(6-38) also reversed ethanol withdrawal-induced anx

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

59 or endocrine response to a subthreshold BNST PACAP infusion.

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

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

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

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

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

65 ponent of the cell size increase elicited by PACAP.

66 neuronal excitability was only increased by PACAP.

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

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

69 cause proarrhythmogenic changes mediated by PACAP and microglia.

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

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

72 hway in neuronal differentiation promoted by PACAP.

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

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

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

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

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

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

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

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

81 tions between the risk genotype, circulating PACAP, and somatic anxiety severity were stronger among

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

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

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

85 To elucidate PACAP interactions, a compendium of microarrays represen

86 t highly dysregulated gene ADCYAP1 (encoding PACAP) was associated with reinnervation and, given that

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

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

89 = 5-8 per group per experiment) to evaluate PACAP plasticity and signaling in nociceptive and stress

90 Exogenous PACAP and substance P initiated a slow depolarization in

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

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

93 CGRP positive neurons expressed PACAP but not glutamate.

94 d sensory neurons expressed the receptor for PACAP and that this peptide could significantly enhance

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

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

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

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

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

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

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

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

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

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

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

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

107 Research in humans implicates PACAP as a useful biomarker for the severity of psychiat

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

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

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

111 No changes in PACAP levels were observed in the central nucleus of the

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 also suggested a potential sex difference in PACAP effects due to differential estrogen regulation of

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

117 pendent) displayed a significant increase in PACAP levels in the bed nucleus of the stria terminalis

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

119 s in the WIN preexposed group, which include PACAP/ADCYAP1.

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

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

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

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 Mice that lack PACAP selectively in neurons of the retrotrapezoid nucle

129 se-dependent manner in vitro [neurite length PACAP 1065.0 um (285.5), vehicle 570.9 mum (181.8), P =

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

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

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

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

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

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

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

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

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

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

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

145 Notably, a postnatal burst of PACAP expression occurred in RTN neurons precisely at th

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 Neonatal mice with deletion of PACAP in RTN neurons displayed increased apnoeas that we

150 hing deficits observed after RTN deletion of PACAP, and suppressed PACAP-evoked respiratory stimulati

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

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

153 he BNST with a normally subthreshold dose of PACAP.

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

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

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

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

158 CO(2)-stimulated breathing; re-expression of PACAP in RTN neurons corrected these breathing deficits.

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

160 Expression of PACAP receptors in neuroendocrine rather than nonneuroen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 uitary adenylate cyclase-activating peptide (PACAP).

188 uitary adenylate cyclase activating peptide, PACAP) being the most strongly upregulated (log2 fold-ch

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 ry adenylate cyclase-activating polypeptide (PACAP), and its cognate receptor, PAC1R, in alcohol with

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

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

212 ry adenylate cyclase-activating polypeptide (PACAP).

213 ry adenylate cyclase-activating polypeptide (PACAP).

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

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

216 ry adenylate cyclase activating polypeptide (PACAP, gene Adcyap1) is a neuropeptide and hormone thoug

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

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

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

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

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

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

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

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

225 Therefore, we examined serum PACAP and associated PAC1R genotype in a cohort of males

226 Since PACAP peptide is cleaved by the human membrane neprilysi

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

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

229 after RTN deletion of PACAP, and suppressed PACAP-evoked respiratory stimulation in the pre-Botzinge

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

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

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

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

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

235 2.5-fold, to 66%, thereby demonstrating that PACAP exerts a powerful inhibitory action on the inducti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

257 ors, and work in rodent models suggests that PACAP manipulation exerts downstream effects on peripher

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 Deletion of the PACAP receptor PAC1 from the pre-Botzinger complex-an RT

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

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

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

276 ntermittent exposure to ethanol recruits the PACAP/PAC1R system of the BNST and that these neuroadapt

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

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

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

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

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

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

283 Thus, PACAP may upregulate excitatory neurotransmission in the

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

285 Our findings demonstrate that well-timed PACAP expression by RTN neurons provides an important su

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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