Species specificity of pharmacological characteristics of CCK-B receptors

Kuwahara, Toshikazu; Kudoh, Tsutomu; Nakano, Atsuko; Yoshizaki, H; Takamiya, Mari; Nagase, Hajime; Arisawa, Mikio

doi:10.1016/0304-3940(93)90597-e

Cited by 13 publications

(6 citation statements)

References 19 publications

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“…A single class of binding sites presenting a high affinity was demonstrated by the binding studies with [ 125 I]‐BH‐[Thr,Nle]CCK‐9. Indeed, the value for the dissociation constant (0.22 nM) is consistent with that obtained for the high affinity sites of the CCK A receptors located in the pancreas of rodents (Sankaran et al , 1980; 1982; Fourmy et al , 1987), dogs (Fourmy et al , 1987), and calves (Le Meuth et al , 1993), and for the CCK B /gastrin receptors located in the pancreas of calves (Le Meuth et al , 1993) or in the cortex of several species (Innis & Snyder, 1980; Saito et al , 1980; Kuwahara et al , 1993). Lower affinity values of [ 125 I]‐BH‐[Thr,Nle]CCK‐9 for CCK B /gastrin receptors in the brain and stomach of guinea‐pigs have been demonstrated (Hunter et al , 1993).…”

Section: Discussionsupporting

confidence: 84%

Pharmacological and biochemical evidence for the simultaneous expression of CCK_B/gastrin and CCK_A receptors in the pig pancreas

Philippe¹,

Lhoste²,

Dufresne

et al. 1997

British J Pharmacology

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In the pig, the secretory response of the pancreas is not inhibited by the antagonist MK329 suggesting that cholecystokininA (CCKA) receptors are not involved. Membranes were isolated from the pancreas of 6 Large White pigs to characterize their CCK receptors. The binding of [M125I]‐BH‐[Thr, Nle]CCK‐9 was dependent on pH, maximal after a 90 min incubation period, saturable and reversible. Saturation analysis of the binding demonstrated a single class of high affinity sites (Kd = 0.22 ± 0.02 nM) and a binding capacity, Bmax= 110.64±12.50 fmol mg−1 protein. Competition binding by agonists and antagonists of CCKA and CCKB/gastrin receptors demonstrated the presence of two distinct binding components, sites presenting a high affinity for [Thr, Nle]CCK‐9, gastrin, PD 135158, L‐365,260 and a low affinity for MK329, SR 27897, and sites presenting a high affinity for [Thr, Nle]CCK‐9, MK329, SR 27897 and a low affinity for gastrin, PD 135158, L‐365,260. These pharmacological data demonstrate the presence of both CCKA and CCKB/gastrin receptors in the pig pancreas, the latter being predominant. Two distinct membrane proteins (50 and 85–100 kDa, respectively) display pharmacological features of CCKB/gastrin and CCKA receptors. In pigs, as in calves and humans, CCKB/gastrin receptors are predominant in the pancreas.

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Section: Discussionsupporting

confidence: 84%

Pharmacological and biochemical evidence for the simultaneous expression of CCK_B/gastrin and CCK_A receptors in the pig pancreas

Philippe¹,

Lhoste²,

Dufresne

et al. 1997

British J Pharmacology

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“…In addition, Josselyn et al (1995) find that administration of a CCKBR antagonist before startle testing (after cued fear acquisition) attenuates fear-potentiated startle. The behavioral differences observed across studies might be attributed to speciesspecific organization of the CCK system (Sekiguchi and Moroji, 1986;Dietl and Palacios, 1989;Kuwahara et al, 1993). In addition, a caveat of our study is the use of a constitutive knockout line with a 129S1 strain background.…”

Section: Discussionmentioning

confidence: 82%

Interaction between the Cholecystokinin and Endogenous Cannabinoid Systems in Cued Fear Expression and Extinction Retention

Bowers

Ressler

2014

Neuropsychopharmacol

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Post-traumatic stress disorder (PTSD) is thought to develop, in part, from improper inhibition of fear. Accordingly, one of the most effective treatment strategies for PTSD is exposure-based psychotherapy. Ideally, neuroscience would inform adjunct therapies that target the neurotransmitter systems involved in extinction processes. Separate studies have implicated the cholecystokinin (CCK) and endocannabinoid systems in fear; however, there is a high degree of anatomical colocalization between the cannabinoid 1 receptor (Cnr1) and CCK in the basolateral amygdala (BLA), a brain region critical for emotion regulation. Although most research has focused on GABA and GABAergic plasticity as the mechanism by which Cnr1 mediates fear inhibition, we hypothesize that a functional interaction between Cnr1 and CCKB receptor (CCKBR) is critical for fear extinction processes. In this study, systemic pharmacological manipulation of the cannabinoid system modulated cued fear expression in C57BL/6J mice after consolidation of auditory fear conditioning. Knockout of the CCKBR, however, had no effect on fear-or anxiety-like behaviors. Nonetheless, administration of a Cnr1 antagonist increased freezing behavior during a cued fear expression test in wild-type subjects, but had no effect on freezing behavior in CCKBR knockout littermates. In addition, we found that Cnr1-positive fibers form perisomatic clusters around CCKBR-positive cell bodies in the BLA. These CCKBR-positive cells comprise a molecularly heterogenous population of excitatory and inhibitory neurons. These findings provide novel evidence that Cnr1 contributes to cued fear expression via an interaction with the CCK system. Dysfunctional Cnr1-CCKBR interactions might contribute to the etiology of, or result from, fear-related psychiatric disease.

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“…Other studies have found a selectivity from 170 (Hughes et al , 1990) to 3,000 (Chang & Lotti, 1986) and intermediate values have also been obtained (Hill & Woodruff, 1990; Akiyama et al , 1996; Taniguchi et al , 1996). The different species used (Kuwahara et al , 1993) and different preparations may account for these discrepancies in selectivity values.…”

Section: Discussionmentioning

confidence: 90%

“…In other studies with radioiodinated peptides, the K d for binding to CCK A and CCK B receptors were slightly lower (e.g. Chang & Lotti, 1986;Kuwahara et al, 1993; see also review by Silvente-Poirot et al, 1993). In binding studies to rat pancreatic CCK A receptors, IQM-95,333 showed a high anity, in the nanomolar range, similar to the typical CCK A antagonist devazepide and approximately 2 ± 3 orders of magnitude higher than lorglumide or the CCK B antagonists, 158.…”

Section: Discussionmentioning

confidence: 90%

Pharmacological evaluation of IQM‐95,333, a highly selective CCK_Areceptor antagonist with anxiolytic‐like activity in animal models

Ballaz

Barber

Fortuño

et al. 1997

British J Pharmacology

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1 The pyridopyrimidine derivative IQM-95,333 ((4aS,5R)-2-benzyl-5-[N a -tert-butoxicarbonyl)L-tryptophyl]amino-1,3dioxoperhydropyrido [1,2-c] 3 Like devazepide, IQM-95,333 was a more potent antagonist of CCK-8S-than of CCK-4-induced contraction of the longitudinal muscle from guinea-pig ileum, suggesting selective antagonism at CCK A receptors. 4 IQM-95,333 and devazepide were also potent inhibitors of CCK-8S-stimulated amylase release from isolated pancreatic acini, a CCK A receptor-mediated e ect. The drug concentrations required (IC 50 s around 20 nM) were higher than in binding studies to pancreas homogenates. 5 Low doses (50 ± 100 mg kg 71 , i.p.) of IQM-95,333 and devazepide, without any intrinsic e ect on food intake or locomotion, blocked the hypophagia and the hypolocomotion induced by systemic administration of CCK-8S, two e ects associated with stimulation of peripheral CCK A receptors. 6 IQM-95,333 showed an anxiolytic-like pro®le in the light/dark exploration test in mice over a wide dose range (10 ± 5,000 mg kg 71 ). Typical CCK A and CCK B antagonists, devazepide and L-365,260 respectively, were only e ective within a more limited dose range. 7 In a classical con¯ict paradigm for the study of anxiolytic drugs, the punished-drinking test, 333,260 were e ective within a narrow dose range. The dose-response curve for the three drugs was biphasic, suggesting that other mechanisms are operative at higher doses. 8 In conclusion, IQM-95,333 is a potent and selective CCK A receptor antagonist both in vitro and in vivo with an anxiolytic-like activity in two di erent animal models, which can only be attributed to blockade of this CCK receptor subtype.

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Species specificity of pharmacological characteristics of CCK-B receptors

Cited by 13 publications

References 19 publications

Pharmacological and biochemical evidence for the simultaneous expression of CCK_B/gastrin and CCK_A receptors in the pig pancreas

Pharmacological and biochemical evidence for the simultaneous expression of CCK_B/gastrin and CCK_A receptors in the pig pancreas

Interaction between the Cholecystokinin and Endogenous Cannabinoid Systems in Cued Fear Expression and Extinction Retention

Pharmacological evaluation of IQM‐95,333, a highly selective CCK_Areceptor antagonist with anxiolytic‐like activity in animal models

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Species specificity of pharmacological characteristics of CCK-B receptors

Cited by 13 publications

References 19 publications

Pharmacological and biochemical evidence for the simultaneous expression of CCKB/gastrin and CCKA receptors in the pig pancreas

Pharmacological and biochemical evidence for the simultaneous expression of CCKB/gastrin and CCKA receptors in the pig pancreas

Interaction between the Cholecystokinin and Endogenous Cannabinoid Systems in Cued Fear Expression and Extinction Retention

Pharmacological evaluation of IQM‐95,333, a highly selective CCKAreceptor antagonist with anxiolytic‐like activity in animal models

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Pharmacological and biochemical evidence for the simultaneous expression of CCK_B/gastrin and CCK_A receptors in the pig pancreas

Pharmacological and biochemical evidence for the simultaneous expression of CCK_B/gastrin and CCK_A receptors in the pig pancreas

Pharmacological evaluation of IQM‐95,333, a highly selective CCK_Areceptor antagonist with anxiolytic‐like activity in animal models