ライフサイエンスコーパス: CCK

1 CCK also increased cell surface-associated NPC1L1 (Niema

2 CCK enhanced phosphatidylinositide 3-kinase (PI3K) and A

3 CCK immunoreactivity in the BNC was observed in somata a

4 CCK is released from DMH neurons in response to repeated

5 CCK is released into blood following a meal; however, th

6 CCK secretion secondary to ILDR1 activation was associat

7 CCK was released in response to peptides and free amino

8 CCK(+)VGluT3(+)INTs exhibit surprising anatomical divers

9 CCK+ axon terminals in the BNC were found both in the ne

10 CCK+ INs in the BNC were morphologically heterogeneous,

11 CCK+ interneurons make stronger synapses onto pyramidal

12 CCK-1R selectivity was achieved mostly by introducing d-

13 CCK-8 assay revealed that no cytotoxicity was observed f

14 CCK-expressing interneurons (CCK+INs) are crucial for co

15 CCK-positive terminals were not established at P21 in th

16 ma GLP-1 (+32%; 95% CI: 23%, 43%; P < 0.01), CCK (+53%, P < 0.01), and NT (+71%, P < 0.01), whereas t

17 ed in 2175 non-agonist ligands of the type 1 CCK receptor (area under curve 78%).

18 Cholecystokinin (CCK) stimulates the type 1 CCK receptor (CCK1R) to elicit satiety after a meal.

19 ocking small molecule agonists to the type 1 CCK receptor were developed using a ligand-guided refine

20 cystokinin (CCK) receptor agonist and type 2 CCK receptor antagonist, GI181771X.

21 tinal epithelial cells with [Thr(28),Nle(31)]CCK increased cholesterol absorption, whereas selective

22 at intravenous injection of [Thr(28),Nle(31)]CCK increased plasma cholesterol levels and intestinal c

23 oendocrine cells of mediators including 5HT, CCK, GLP-1, PYY and ghrelin that act on vagal afferent n

24 hologic concentrations of cholecystokinin-8 (CCK).

25 -treatment enhanced Ca(2+) mobilization by a CCK agonist (CCK-8s).

26 tion of CCK(NTS) neurons to be mediated by a CCK(NTS)-->PVH pathway that also encodes positive valenc

27 lective CCK-2R agonist by replacing Gly in a CCK-8 derivative with Glu.

28 whereas their activation mimics the CRR in a CCK-dependent manner.

29 ther analyse in vivo signalling interplay, a CCK-1 antagonist (lorglumide) was intraperitoneally inje

30 terminals, indicative of the existence of a CCK interneuronal network.

31 CTSB deletion also abolished CCK-induced caspase 3 activation, apoptosis-inducing fac

32 hen show that vHPC inputs primarily activate CCK+ and PV+ interneurons, with weaker connections onto

33 After CCK infusion in mPFC, we optogenetically stimulated mPFC

34 However, these particular before and after CCK treatment values did not achieve statistical signifi

35 hanced Ca(2+) mobilization by a CCK agonist (CCK-8s).

36 All CCK+ somata gave rise to 2-4 dendrites that branched spa

37 feeding following administration of amylin, CCK, and LiCl, but not LPS.

38 the appetite suppressing effects of amylin, CCK, and LiCl, but not LPS.

39 previously demonstrated that both GLP-1 and CCK are produced in the endocrine pancreas of obese mice

40 d peptide compared with the stable GLP-1 and CCK mimetics exendin-4 and (pGlu-Gln)-CCK-8, respectivel

41 at mouse pancreatic islets secrete GLP-1 and CCK, but only GLP-1 acts locally within the islet to pro

42 CD36 mice released less secretin (-60%) and CCK (-50%) compared with wild-type mice.

43 Both CALCA and CCK neurons project rostrally to the preoptic hypothalam

44 Cch and CCK-8 both dose-dependently stimulated secretory respons

45 ics.Broad ranges of cellular cholesterol and CCK responsiveness were observed, with elevated choleste

46 etween the cannabinoid 1 receptor (Cnr1) and CCK in the basolateral amygdala (BLA), a brain region cr

47 adaptations in mPFC involving DeltaFosB and CCK through cortical projections to distinct subcortical

48 Ethanol and CCK activated MPTP through different mechanisms-ethanol

49 The effects of ethanol and CCK were mediated by MPTP because they were not observed

50 pD(-/-) mice by a combination of ethanol and CCK.

51 reatitis after administration of ethanol and CCK.

52 released more secretin (3.5- to 4-fold) and CCK (2- to 3-fold), generated more cAMP (2- to 2.5-fold)

53 ether, these results suggest that leptin and CCK receptors may both contribute to short-term satiety,

54 relin inhibits currents evoked by leptin and CCK-8, which operate through independent ionic channels.

55 s and inhibits currents evoked by leptin and CCK-8.

56 de, as a result of oxidative metabolism, and CCK by increasing cytosolic Ca(2+).

57 ) showed similar in vitro CCK-1R potency and CCK-1R affinity as CCK-8, very high selectivity for CCK-

58 etected on apical membranes of secretin- and CCK-positive EECs and colocalized with cytosolic granule

59 vitro CCK-1R potency and CCK-1R affinity as CCK-8, very high selectivity for CCK-1R over the cholecy

60 eal-time PCR, western blots, scratch assays, CCK-8 assays and tubule formation assays.

61 CCK1R and CCK2R with antagonists attenuated CCK-induced cholesterol absorption.

62 Inhibition or knockdown of NPC1L1 attenuated CCK-induced cholesterol absorption.

63 Ligation of the bile duct, blocking CCK receptors with proglumide or inhibition of Niemann-P

64 In the rat BNC CCK is expressed in two separate IN subpopulations, term

65 PFC, highlighting unexpected roles for both CCK+ interneurons and endocannabinoid modulation in hipp

66 ry responses and exocytotic events evoked by CCK-8 were mediated by CCK-A and not CCK-B receptors.

67 l dystroglycan for functional innervation by CCK-positive basket cell axon terminals was confirmed by

68 The number of inhibitory synapses made by CCK(+)VGlut3(+) basket cells and the inhibitory drive th

69 otic events evoked by CCK-8 were mediated by CCK-A and not CCK-B receptors.

70 ugh mechanisms mediated, at least partly, by CCK.

71 in potentiates vagal afferent stimulation by CCK but this is lost in obesity.

72 Isoprenaline rapidly stimulated cardiac CCK gene expression in vitro and in vivo, which suggests

73 itory cholecystokinin-positive basket cells (CCK(+) BCs), through enhanced inhibition of GABA release

74 the cholecystokinin-expressing basket cells (CCK-BC).

75 In Caco-2 cells, CCK enhanced CCK1R/CCK2R heterodimerization.

76 roduct distinct from intestinal and cerebral CCK peptides.

77 Cholecystokinin (CCK) and leptin are satiety-controlling peptides, yet th

78 Cholecystokinin (CCK) increased the activity of CTSB, cathepsin L, trypsi

79 Cholecystokinin (CCK) is a neuropeptide expressed in neurons in the dorso

80 Cholecystokinin (CCK) is a peptide hormone that induces bile release into

81 Cholecystokinin (CCK) is a satiety hormone produced by discrete enteroend

82 Cholecystokinin (CCK) is an important satiety factor, acting at type 1 re

83 Cholecystokinin (CCK) neurons located deeper within the dorsal horn (lami

84 Cholecystokinin (CCK) stimulates the type 1 CCK receptor (CCK1R) to elici

85 ule ligand that is a type 1 cholecystokinin (CCK) receptor agonist and type 2 CCK receptor antagonist

86 gon-like peptide-1 (GLP-1), cholecystokinin (CCK) and oxyntomodulin (OXM) as treatments for obesity-d

87 that a non-biased agonist, cholecystokinin (CCK) induces conformational states of the CCK2R activati

88 leptin receptor (LepRb) and cholecystokinin (CCK) (PBN LepRb(CCK) neurons), which project to the vent

89 -like peptide 1 (GLP-1) and cholecystokinin (CCK) are gut-derived peptide hormones known to play impo

90 -like peptide-1 (GLP-1) and cholecystokinin (CCK) exert important complementary beneficial metabolic

91 umably parvalbumin (PV) and cholecystokinin (CCK) expressing basket interneurons.

92 e for total GLP-1, GIP, and cholecystokinin (CCK) in plasma.

93 5-HT and cholecystokinin (CCK) induced dose-dependent increases in VAN activity in

94 creted by the pancreas, and cholecystokinin (CCK), secreted by the small intestine.

95 (SOM), calretinin (CR), and cholecystokinin (CCK).

96 agonist carbachol (Cch) and cholecystokinin (CCK-8), including 1) amylase secretion, 2) exocytosis, 3

97 Gut hormones, such as cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1), are released f

98 exigenic molecules, such as cholecystokinin (CCK) and leptin, to stimulate feeding.

99 exigenic molecules, such as cholecystokinin (CCK) and leptin, to stimulate feeding.

100 interactions exist between cholecystokinin (CCK)-expressing hilar commissural associational path (HI

101 of DMV neurones excited by cholecystokinin (CCK) was unaltered but the proportion of neurones in whi

102 t of NTS neurons containing cholecystokinin (CCK(NTS)) is responsive to nutritional state and that th

103 boxylase 1 (GAD1) in either cholecystokinin (CCK)- or neuropeptide Y (NPY)-expressing interneurons.

104 perisomatic inhibition from cholecystokinin (CCK)-expressing interneurons.

105 notropic polypeptide (GIP), cholecystokinin (CCK), peptide YY (PYY), and neurotensin (NT)] and on glu

106 classic intestinal hormone cholecystokinin (CCK) in amounts similar to those in the intestine and br

107 with the intestinal hormone cholecystokinin (CCK-8).

108 everal of the gut hormones (cholecystokinin (CCK); peptide YY3-36 (PYY3-36); glucagon-like peptide-1

109 Here we identify cholecystokinin (CCK) and noradrenergic, dopamine beta-hydroxylase (DBH)-

110 rotonin 5-HT1B receptors in cholecystokinin (CCK) inhibitory interneurons of the mammalian dentate gy

111 loss of TrkB signalling in cholecystokinin (CCK)-GABAergic neurons induces glucocorticoid resistance

112 B1R+) interneurons - mainly cholecystokinin (CCK)-expressing cells.

113 of endogenous neuropeptide cholecystokinin (CCK), released from dentate CCK interneurons, in regulat

114 ly express the neuropeptide cholecystokinin (CCK), to two groups of spatially segregated GABAergic in

115 at express the neuropeptide cholecystokinin (CCK).

116 etylcholine (ACh)-, but not cholecystokinin (CCK)-induced Ca(2+) oscillations in a concentration-depe

117 es FA-mediated secretion of cholecystokinin (CCK) and secretin, peptides released by enteroendocrine

118 lly increased expression of cholecystokinin (CCK) in regenerating muscle from Trim33 knockout mice, s

119 port examines the effect of cholecystokinin (CCK) on plasma cholesterol level and intestinal choleste

120 ease of the satiety peptide cholecystokinin (CCK) in the brain.

121 ning the anxiogenic peptide cholecystokinin (CCK), we also examined whether the PCP-induced social wi

122 ns that express the peptide cholecystokinin (CCK).

123 ed continuously, and plasma cholecystokinin (CCK), ghrelin, and glucagon-like peptide-1 (GLP-1) conce

124 etion of the fat-stimulated cholecystokinin (CCK) hormone in the small intestine, while ILDR1 in EpH4

125 ancreatitis by supramaximal cholecystokinin (CCK-8) stimulation inhibits VAMP8-mediated mid- and late

126 We first show that cholecystokinin (CCK+), parvalbumin (PV+), and somatostatin (SOM+) expres

127 studies have implicated the cholecystokinin (CCK) and endocannabinoid systems in fear; however, there

128 hway was independent of the cholecystokinin (CCK) stimulation pathway.

129 ly through induction of the cholecystokinin (CCK)-B receptor: CCKB blockade in mPFC induces a resilie

130 orn to CB-treated dams exhibited compromised CCK-INT-mediated feedforward and feedback inhibition.

131 We unequivocally demonstrate CCK(+)VGluT3(+)INT-mediated GABA/glutamate cotransmissio

132 cholecystokinin (CCK), released from dentate CCK interneurons, in regulating neurogenic niche cells a

133 In contrast, reducing dentate CCK induces reactive astrocytes, which correlates with d

134 tein betagamma dimer (Gbetagamma) diminished CCK-induced PI3K and Akt phosphorylation.

135 PI3K and Akt or knockdown of PI3K diminished CCK-induced NPC1L1-Rab11a interaction and cholesterol ab

136 1R and CCK2 or either one of them diminished CCK-induced cholesterol absorption to the same extent.

137 antibody directed at GFRAL or by disrupting CCK neuronal signalling.

138 l conditions, GABAergic inhibition dominates CCK(+)VGluT3(+)INT signaling, glutamatergic signaling be

139 ut there is no information on how endogenous CCK alters synaptic properties.

140 here are clear demonstrations that exogenous CCK modulates food intake and neuropeptide expression in

141 l cells and human Caco-2 cells; both express CCK receptor 1 and 2 (CCK1R and CCK2R).

142 cortical circuits of basket cells expressing CCK and vesicular glutamate transporter 3 (VGlut3).

143 nalog, and anisotropy of a bound fluorescent CCK analog.

144 summary, our data suggest no direct role for CCK in stimulating insulin secretion and highlight the c

145 y at IT cells, confirming a central role for CCK+ interneurons.

146 related radioiodinated ligands selective for CCK receptor subtypes that utilize the same allosteric l

147 affinity as CCK-8, very high selectivity for CCK-1R over the cholecystokinin 2 receptor (CCK-2R), str

148 Inhibition of GABA release from CCK neurons disinhibits parvalbumin (PV) interneurons an

149 GIP, CCK and OXM molecules appear to offer promising new clas

150 istration of the peptides, except (pGlu-Gln)-CCK-8 alone, in combination with glucose significantly l

151 pGlu-Gln)-CCK-8/exendin-4 hybrid, (pGlu-Gln)-CCK-8 alone, or (pGlu-Gln)-CCK-8 in combination with exe

152 ybrid, (pGlu-Gln)-CCK-8 alone, or (pGlu-Gln)-CCK-8 in combination with exendin-4 for 21 days to high-

153 -1 and CCK mimetics exendin-4 and (pGlu-Gln)-CCK-8, respectively.

154 HbA1c was reduced in the (pGlu-Gln)-CCK-8/exendin-4 hybrid and combined parent peptide treat

155 nd therapeutic utility of a novel (pGlu-Gln)-CCK-8/exendin-4 hybrid peptide compared with the stable

156 daily administration of the novel (pGlu-Gln)-CCK-8/exendin-4 hybrid, (pGlu-Gln)-CCK-8 alone, or (pGlu

157 ovide novel circuit-based information on how CCK acts on local astrocytes to regulate the key behavio

158 However, CCK+ inputs undergo depolarization-induced suppression o

159 (CCK1Rs) on vagal afferent neurons; however, CCK agonists have failed clinical trials for obesity.

160 Our study therefore identifies CCK neurons as a novel and critical cellular component o

161 ation of GABA(B)R-mediated autoinhibition in CCK(+) BCs promotes aberrant high frequency oscillations

162 intestine, ILDR1 is expressed exclusively in CCK cells.

163 nalyses revealed that suppression of GAD1 in CCK+ interneurons resulted in locomotor and olfactory se

164 t did not alter plasma cholesterol levels in CCK-treated mice.

165 n products and study their ability to induce CCK and GLP-1 release in enteroendocrine STC-1 cells.

166 However, Trim33 knockdown induced CCK expression in muscle, suggesting that suppression of

167 o be fully responsible for olive oil-induced CCK secretion.

168 cystokinin expressing cortical interneurons (CCK(+)VGluT3(+)INTs) has prompted speculation of GABA/gl

169 CCK-expressing interneurons (CCK+INs) are crucial for controlling hippocampal activit

170 on cholecystokinin-expressing interneurons (CCK-INTs), a prominent CB subtype-1 receptor (CB1R) expr

171 containing receptor 1 (ILDR1) in intestinal CCK cells and postulated that this receptor conveyed the

172 Additionally, we provide evidence that islet CCK expression is regulated by glucose, but its receptor

173 wo separate IN subpopulations, termed large (CCK(L) ) and small (CCK(S) ).

174 PBN LepRb(CCK) neurons are a crucial component of the CRR system a

175 (LepRb) and cholecystokinin (CCK) (PBN LepRb(CCK) neurons), which project to the ventromedial hypotha

176 In addition, many CCK+ neurons were contacted by multiple CCK+ terminals,

177 atiety, and leptin could positively modulate CCK signalling.

178 many CCK+ neurons were contacted by multiple CCK+ terminals, indicative of the existence of a CCK int

179 This is true for natural CCK, as well as ligands with distinct chemistries and ac

180 ypercholesterolemic effect of [Thr28, Nle31]-CCK in LDLR(-/-) mice.

181 The same dose of [Thr28, Nle31]-CCK induced 6 and 13% increases in plasma triglyceride a

182 eficient T190M dystroglycan displayed normal CCK-positive terminals.

183 oked by CCK-8 were mediated by CCK-A and not CCK-B receptors.

184 bition (H-89) blunted secretin (80%) but not CCK release, which was reduced (50%) by blocking of calm

185 T-0632 fully inhibited binding and action of CCK at this receptor, while exhibiting no saturable bind

186 Activation of CCK neurons also promoted NREM sleep.

187 Optogenetic activation of CCK(NTS) axon terminals within the PVH reveal the satiat

188 on, induced by physiologic concentrations of CCK, into a sustained decrease in DeltaPsim, resulting i

189 A moderate density of CCK+ INs was found in all nuclei of the BNC.

190 the body, this report examined the effect of CCK on increasing plasma cholesterol and triglycerides i

191 projections blocked the anxiogenic effect of CCK, although no effect was observed on other symptoms o

192 ons would rescue the pathological effects of CCK in mPFC.

193 he pancreatic beta-cells, direct evidence of CCK promoting insulin release in human islets remains to

194 This could explain the failure of CCK agonists in previous clinical trials and supports th

195 ecifically increases the firing frequency of CCK-positive but not parvalbumin-positive interneurons a

196 hin the PVH reveal the satiating function of CCK(NTS) neurons to be mediated by a CCK(NTS)-->PVH path

197 Finally, inhibition of CCK neurons mimics the antidepressant behavioral effects

198 sion of ZGs contributes to the initiation of CCK-induced pancreatic injury, and that blockade of this

199 e results suggest that normal integration of CCK(+) basket cells in cortical networks is key to suppo

200 ab11a (Rab-GTPase-11a), whereas knockdown of CCK receptors or inhibition of G protein betagamma dimer

201 tion of fatty acids elevated blood levels of CCK in wild-type mice but not Ildr1-deficient mice, alth

202 5,212-2 (WIN) produced a significant loss of CCK-INTs in the offspring.

203 troglycan, in pyramidal cells caused loss of CCK-positive basket cell terminals in hippocampus and ne

204 oglycan in both formation and maintenance of CCK-positive terminals.

205 from deficient CB(1)-mediated modulation of CCK transmission.

206 ent study the distribution and morphology of CCK+ INs and their axon terminals in the BNC of the monk

207 These data indicate that the morphology of CCK+ INs in the monkey is very similar to that of the ra

208 ontexts where the glutamatergic phenotype of CCK(+)VGluT3(+)INTs is amplified, they promote paradoxic

209 We found two firing phenotypes of CCK+INs in rat hippocampal CA3 area; either possessing a

210 nstead of Asp at the penultimate position of CCK-8.

211 biota, thereby stimulating the production of CCK from the EECs possibly in response to propionate.

212 histochemistry showed major up-regulation of CCK in enteroendocrine cells (EECs) that were glucagon-l

213 n ILDR1-transfected CHO cells and release of CCK from isolated intestinal cells required a unique com

214 e first report of somatodendritic release of CCK in the brain in male Sprague Dawley rats.

215 ition through the somatodendritic release of CCK.

216 s important to take into account the role of CCK-BC in the generation and information processing of t

217 data identify the functional significance of CCK(NTS) neurons and reveal a sufficient and discrete NT

218 Ingested fat is the major stimulant of CCK secretion.

219 h is associated with a marked stimulation of CCK and suppression of ghrelin.

220 Interestingly, the Maf(+) subset of CCK neurons is composed of transient vesicular glutamate

221 on in muscle, suggesting that suppression of CCK expression requires Trim33.

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

223 echanisms of two previously unknown types of CCK+INs and demonstrate that alternative splicing of few

224 t of a patient's own cellular environment on CCK stimulus-activity coupling and to determine whether

225 re, we tested whether islet-derived GLP-1 or CCK is necessary for the full stimulation of insulin sec

226 a prevented ghrelin inhibition of leptin- or CCK-8-evoked vagal firing.

227 ed hemoglobin in obese and diabetic patients.CCK responsiveness varies widely across the population,

228 r effects than tricaprylin on AUCs of plasma CCK (+40%, P < 0.01) and NT (+32%, P < 0.01), but not GL

229 C12 + Trp: 1,056 +/- 106), stimulated plasma CCK (AUC(area under the curve)0-90 min, pmol/L*min; cont

230 al and duodenal pressures; stimulated plasma CCK, GLP-1, GIP, insulin, and glucagon (all r > 0.57, P

231 protein load, antropyloroduodenal pressures, CCK, GLP-1, and glucagon did not differ between lean and

232 trate that the mammalian heart expresses pro-CCK in amounts comparable to natriuretic prohormones and

233 tive PCR, a library of sequence-specific pro-CCK assays, peptide purification, and mass spectrometry,

234 ests that the cardiac-specific truncated pro-CCK may have pathophysiological relevance as a new marke

235 Distal (GLP-1/PYY/NT), but not proximal (CCK/GIP), enteroendocrine responses were generally great

236 sh neuropeptides found in the mammalian PVN (CCK, CRH, ENK, NTS, SS, VIP, OXT, AVP), we provide the f

237 rations of the gut hormones GLP-1, GIP, PYY, CCK and insulin did not offer an explanation of the diff

238 highly selective cholecystokinin 1 receptor (CCK-1R) agonists with the potential to treat obesity has

239 CCK-1R over the cholecystokinin 2 receptor (CCK-2R), strong reduction of food intake in lean pigs fo

240 Reduced CCK sensitivity best correlated with elevated serum trig

241 elevated cholesterol correlated with reduced CCK sensitivity.

242 NC, there is almost no information regarding CCK+ INs in these species.

243 se findings demonstrate that ILDR1 regulates CCK release through a mechanism dependent on fatty acids

244 ptic actions of somatodendritically released CCK in the hypothalamus and reveal a new form of retrogr

245 ated suppression of inhibition from residual CCK-INTs and displayed altered social behavior.

246 Further, residual CCK-INTs in animals prenatally treated with WIN displaye

247 ion of corticoaccumbens projections reversed CCK-induced social avoidance and sucrose preference defi

248 In addition, we found a highly selective CCK-2R agonist by replacing Gly in a CCK-8 derivative wi

249 at three gastrointestinal signals-serotonin, CCK, and PYY-are necessary or sufficient for these effec

250 ing on the nerves within the pancreas slice, CCK cellular actions directly affected human acinar cell

251 pulations, termed large (CCK(L) ) and small (CCK(S) ).

252 tically target GABAergic axo-axonic and some CCK interneurons in restricted septo-temporal CA3 segmen

253 C12 and Trp each stimulated CCK (P < 0.05), but to a lesser degree than C12 + Trp, a

254 eptor conveyed the signal for fat-stimulated CCK secretion.

255 Only olive oil stimulated CCK release.

256 Specifically, stimulating CCK release supports neurogenic proliferation of NSCs th

257 Knockdown of Rab11a suppressed CCK-induced NPC1L1 translocation and cholesterol absorpt

258 Supramaximal CCK-8 (60 min) caused a 60% reduction in the expression

259 tant to secretory inhibition by supramaximal CCK-8, and despite a 4.5-fold increase in total cellular

260 Elevation of cAMP during supramaximal CCK-8 mitigates third-phase secretory inhibition and aci

261 hanced secretion in response to supramaximal CCK-8 and prevented accumulation of activated trypsin.

262 wever, when stimulated with supraphysiologic CCK-8 levels to mimic pancreatitis, Munc18c-depleted (Mu

263 omponent was selectively reduced at SynII(-) CCK interneurons.

264 sed on systematic investigation of synthetic CCK-8 analogues with N-terminal linkage to fatty acids.

265 sing subsets of all known dendrite targeting CCK(+) interneurons in addition to the expected basket c

266 e neuropeptide cholecystokinin-tetrapeptide (CCK-4) in 16 healthy male subjects in a double-blind, pl

267 These data imply that CCK enhances cholesterol absorption by activation of a p

268 Our optogenetic results reveal that CCK and DBH neurons in the NTS directly engage CGRP(PBN)

269 l-specific anterograde tracing revealed that CCK(NTS) neurons provide a distinctive innervation of th

270 These findings suggest that CCK-increased plasma cholesterol and triglycerides as a

271 The CCK interneurons provide a surprisingly strong feedforwa

272 The CCK-4 induced anxiety and elicited widely distributed ac

273 e but not Ildr1-deficient mice, although the CCK secretory response to trypsin inhibitor was retained

274 tterns were determined before and during the CCK-4-challenge without pretreatment and after treatment

275 However, the CCK-containing subgroup increased in number, whereas the

276 Moreover, the reduction in the CCK-4 induced activation of the rACC correlated with the

277 e 2-positive interneurons, which include the CCK-expressing basket cells, strongly suppressed inhibit

278 y, we examined the cardiac expression of the CCK gene in adult mammals and its expression at the prot

279 itatory macrocircuit by the silencing of the CCK inhibitory microcircuit.

280 h-evoked responses did not affect any of the CCK-8-evoked responses, indicating that rather than acti

281 get for benzodiazepines and suggest that the CCK-4/fMRI paradigm might represent a human translationa

282 Using the CCK-8 cell proliferation assay, cell cycle analysis, and

283 fear expression via an interaction with the CCK system.

284 8c(+/-) mice after hyperstimulation with the CCK-8 analog caerulein.

285 also see no increase in GSIS in response to CCK peptides.

286 in all rats; HFD attenuated the response to CCK, but not 5-HT.

287 cates fMRI brain imaging of CNS responses to CCK and ghrelin is feasible, informative and provides op

288 ition and intracellular calcium responses to CCK.

289 4R(PVH)) cells, which are also responsive to CCK.

290 phobic negatively charged peptides triggered CCK release, while the highest GLP-1 response was found

291 of breast cancer cells were determined using CCK-8 and Hoechst 33342 assays and flow cytometry, after

292 compound 9 (NN9056) showed similar in vitro CCK-1R potency and CCK-1R affinity as CCK-8, very high s

293 mPFC induces a resilient phenotype, whereas CCK administration into mPFC mimics the anxiogenic- and

294 gainst phosphorylated STAT3 (pSTAT3) whereas CCK-8s reduced leptin-induced nuclear pSTAT3 accumulatio

295 s-activity coupling and to determine whether CCK sensitivity correlated with the metabolic phenotype

296 ered but the proportion of neurones in which CCK increased excitatory glutamatergic synaptic inputs w

297 MORs in CA1 are not usually associated with CCK-expressing cells.

298 activation of the rACC after challenge with CCK-4 (p<.005, corrected for multiple comparisons) and i

299 ard clinical metric correlated directly with CCK responsiveness.

300 ar pSTAT3 was reduced by co-stimulation with CCK-8s.