ライフサイエンスコーパス: CCK

1 CCK activates NTS-PPG cells by a circuit involving adren

2 CCK also increased cell surface-associated NPC1L1 (Niema

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

4 CCK has been shown to act as an endogenous "anti-analges

5 CCK has highly cell-type-selective effects even within t

6 CCK is involved in regulating insulin secretion and gluc

7 CCK is released from DMH neurons in response to repeated

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

9 CCK secretion secondary to ILDR1 activation was associat

10 CCK-KO mice fed a low-fat diet had a reduced acute insul

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

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

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

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

15 l types including gastrin-, glucagon/GLP-1-, CCK-, secretin-producing cell populations and an increas

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

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

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

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

20 hologic concentrations of cholecystokinin-8 (CCK).

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

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

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

24 After CCK infusion in mPFC, we optogenetically stimulated mPFC

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

26 agonist (Sp-cAMPS) or CCK1 receptor agonist (CCK-8).

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

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

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

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

31 ith delta and mu opioid agonist activity and CCK antagonist activity within one molecule offer a nove

32 complementary coiled-coil peptides, CCE and CCK, forming antiparallel heterodimers; Fab' fragment of

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

34 e distributions of cholecystokinin (CCK) and CCK receptors in the central nervous system (CNS) overla

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

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

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

38 Ethanol and CCK activated MPTP through different mechanisms-ethanol

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

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

41 reatitis after administration of ethanol and CCK.

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

43 dies showed that a combination of leptin and CCK-8 caused a significant increase in membrane input re

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

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

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

47 as higher in CCK-KO than wild-type mice, and CCK-KO mice had greater oxidation of carbohydrates while

48 only one (control) or both (target) MSH and CCK receptors.

49 However, CB(1)R and CCK-positive GABAergic terminals are present on pyramida

50 Likewise, diminished secretin and CCK responses to FA were observed with CD36 intestinal s

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

52 o distinct opioid receptors and antagonizing CCK receptors in the CNS.

53 demonstrate that an abundant ligand such as CCK can signal through the same receptor in different ne

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

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

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

57 This involves the interaction between CCK/Src/PI3K cascades and leptin/JAK2/PI3K/STAT3 signali

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

59 Both CCK and epinephrine acted to increase glutamatergic tran

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

61 PPG neurons in the NTS were excited by CCK and epinephrine, but not by the melanocortin recepto

62 to acetaldehyde and ethyl oleate followed by CCK-8 stimulation mildly perturbed the actin cytoskeleto

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

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

65 and that this inversion could be mediated by CCK within the CNS.

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

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

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

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

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

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

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

73 roduct distinct from intestinal and cerebral CCK peptides.

74 Cholecystokinin (CCK) can stimulate exocrine secretion by acting directly

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

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

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

78 Cholecystokinin (CCK) is a potent regulator of visceral functions as a co

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

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

81 Cholecystokinin (CCK) is released in response to lipid intake and stimula

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

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

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

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

86 on-like peptide 1 analogue, cholecystokinin (CCK) and pancreatic polypeptide (PP).

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

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

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

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

91 5-HT and cholecystokinin (CCK) induced dose-dependent increases in VAN activity in

92 tain melanocortin (MSH) and cholecystokinin (CCK) pharmacophores that are connected via a fluorescent

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

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

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

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

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

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

99 tic acini to ethanol blocks cholecystokinin (CCK)-8-stimulated apical exocytosis and redirects exocyt

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

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

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

103 rom basket cells expressing cholecystokinin (CCK(b) cells) and parvalbumin (PV(b) cells), respectivel

104 ufficient and necessary for cholecystokinin (CCK) signaling to trigger vagal afferent firing and regu

105 nnels, whereas release from cholecystokinin (CCK)-containing interneurons is generated by microdomain

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

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

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

109 Another satiety hormone, cholecystokinin (CCK), has also been linked to activation of brain stem n

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

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

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

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

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

115 ally important neuropeptide cholecystokinin (CCK) is able to selectively depolarize PV+ basket cells,

116 at express the neuropeptide cholecystokinin (CCK).

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

118 The distributions of cholecystokinin (CCK) and CCK receptors in the central nervous system (CN

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

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

121 -transduction decoupling of cholecystokinin (CCK), a physiological agonist for small intestinal propu

122 ric oxide synthase (NOS) or cholecystokinin (CCK), which are known to be physiologically and developm

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

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

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

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

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

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

129 e two basket cell classes, cholecystokinin- (CCK) and parvalbumin (PV)-containing basket cells, begin

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

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

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

133 1R and CCK2 or either one of them diminished CCK-induced cholesterol absorption to the same extent.

134 whereas duodenal Sp-cAMPS bypassed duodenal CCK resistance and activated duodenal PKA and lowered gl

135 duodenal PKA blocked the ability of duodenal CCK-8 to reduce glucose production in control rats, wher

136 itoneal stimuli that do not typically elicit CCK release suggests that this hormone has chronic effec

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

138 uropathic pain conditions promote endogenous CCK release in CNS regions of pain modulation.

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

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

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

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

143 making these cells sensitive biosensors for CCK.

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

145 engths of PFC pyramidal cell inhibition from CCK(b) and PV(b) cells that may underlie cortical oscill

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

147 CCK-induced depression of GABA release from CCK+ basket cells.

148 ar alterations that regulate signalling from CCK(b) and PV(b) cells.

149 ects on waist circumference regain; in GHRL, CCK, MLXIPL, and LEPR on weight; in PPARC1A, PCK2, ALOX5

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

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

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

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

154 -1 and CCK mimetics exendin-4 and (pGlu-Gln)-CCK-8, respectively.

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

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

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

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

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

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

161 wer CCK and cannabinoid 1 receptor (CB1R) in CCK(b) cells, and lower glutamic acid decarboxylase 67 (

162 The increased plasma cholesterol in CCK-treated mice was distributed in very-low, low and hi

163 LTP is not elicited in CCK-expressing Schaffer collateral-associated cells, whi

164 intestine, ILDR1 is expressed exclusively in CCK cells.

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

166 Energy expenditure was higher in CCK-KO than wild-type mice, and CCK-KO mice had greater

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

168 ce of small GTPases such as RhoA and Rac1 in CCK-induced pancreatic secretion is also described.

169 The deficiency of insulin secretion in CCK-KO mice was not associated with changes in beta-cell

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

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

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

173 and insulin secretion of CCK gene knockout (CCK-KO) mice and their wild-type controls using intraper

174 llectively known as the cyclic cystine knot (CCK) motif.

175 ed structure known as a cyclic cystine knot (CCK).

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

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

178 Leptin/CCK-8 synergistically stimulated a 7.7-fold increase in

179 ular signaling pathways that modulate leptin/CCK synergism.

180 e abolished the synergistic action of leptin/CCK-8 on neuronal firing.

181 and PI3K genes resulted in a loss of leptin/CCK-stimulated pSTAT3.

182 mine the effect of these molecules on leptin/CCK synergism.

183 o investigate the neuronal circuitry linking CCK to the population of NTS-PPG neurons.

184 These alterations include lower CCK and cannabinoid 1 receptor (CB1R) in CCK(b) cells, a

185 pression of the enteroendocrine cell markers CCK, secretin and glucagon while expression of a pan-int

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

187 that intravenous injection of [Thr28, Nle31]-CCK at a dose of 50 ng/kg significantly increased plasma

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

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

190 eficient T190M dystroglycan displayed normal CCK-positive terminals.

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

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

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

194 signaling abolished the excitatory action of CCK.

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

196 Administration of CCK into nuclei of the rostral ventromedial medulla indu

197 conjugate, followed by the administration of CCK-P produced long-term survivors in SCID (C.B.-17) mic

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

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

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

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

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

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

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

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

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

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

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

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

210 5,212-2 (WIN) produced a significant loss of CCK-INTs in the offspring.

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

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

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

214 is a major mediator of FA-induced release of CCK and secretin.

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

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

217 ition through the somatodendritic release of CCK.

218 sed and decreased strength, respectively, of CCK(b) and PV(b) cell-mediated inhibition of postsynapti

219 current controversies regarding the role of CCK to control gastric function via vago-vagal reflexes.

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

221 died plasma glucose and insulin secretion of CCK gene knockout (CCK-KO) mice and their wild-type cont

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

223 Ingested fat is the major stimulant of CCK secretion.

224 us release was generated at the terminals of CCK-expressing interneurons.

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

226 of the same pathologic effects of ethanol on CCK-8-stimulated exocytosis in pancreatic acini.

227 ane input resistance compared with leptin or CCK-8 alone.

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

229 ly expressing CD36 did not alter secretin or CCK release, consistent with a minimal effect of adjacen

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

231 s, exemplified by the effects of the peptide CCK, dynamically enhance the differential functions of t

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

233 s conjugated in multiple grafts to polyHPMA (CCK-P; P is the HPMA copolymer backbone).

234 ed by Aspergillus alliaceus are known potent CCK(A) antagonists.

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

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

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

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

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

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

241 reflex is more sensitive in the fasted rat, CCK amplifies this sensitivity.

242 ed through a G(q)/G(12/13)-coupled receptor, CCK(A), and is attenuated by inhibitors of p38 mitogen-a

243 Acetaldehyde and ethyl oleate redirected CCK-8-stimulated exocytosis to the basal and lateral pla

244 Reduced CCK sensitivity best correlated with elevated serum trig

245 e, ethyl palmitate, and ethyl oleate reduced CCK-8-stimulated apical exocytosis and formation of apic

246 elevated cholesterol correlated with reduced CCK sensitivity.

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

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

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

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

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

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

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

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

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

256 Only olive oil stimulated CCK release.

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

265 e recorded interneurons, to demonstrate that CCK acts via G-protein-coupled CCK2 receptors to engage

266 We hypothesized that CCK deficiency would alter the regulation of insulin sec

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

276 poAI levels were significantly higher in the CCK-treated mice than in untreated control mice.

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 V+ basket cells, but it had no effect on the CCK-induced depression of GABA release from CCK+ basket

282 olaceae, and Fabaceae families and share the CCK motif with trypsin-inhibitory knottins from a plant

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

284 ver, the molecular mechanisms underlying the CCK-induced selective and powerful excitation of PV+ bas

285 gesting either convergent evolution upon the CCK structure or movement of cyclotide-encoding sequence

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

287 fear expression via an interaction with the CCK system.

288 8c(+/-) mice after hyperstimulation with the CCK-8 analog caerulein.

289 rgeting bistratified cells do not respond to CCK.

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

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

292 ition and intracellular calcium responses to CCK.

293 4R(PVH)) cells, which are also responsive to CCK.

294 when fed a high-fat diet (HFD) for 10 weeks, CCK-KO mice developed glucose intolerance despite increa

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

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

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

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

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

300 ard clinical metric correlated directly with CCK responsiveness.

301 olites (1-3 mmol/L) and then stimulated with CCK-8.