Demonstration of a putative receptor site for cholecystokinin in rat brain

Hays, Sally E.; Beinfeld, Margery C.; Jensen, Robert T.; Goodwin, Frederick K.; Paul, Steven M.

doi:10.1016/0143-4179(80)90009-8

Cited by 177 publications

(31 citation statements)

References 15 publications

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“…The present results add further support to the view that, just as there is a family of CCK-gastrin peptides, there is also a family of related cell surface receptors for CCK and gastrin. This family of receptors includes a receptor on the pancreatic acinar cell that has a much higher affinity for CCK than G17 (32,33), a receptor in the brain that has a moderate preference for CCK over G17 (34,35), and the canine parietal cell receptor that has an equal affinity for CCK8 and G17. Antral smooth muscle cell responses to gastrin and CCK also indicate the presence of a receptor with equal affinity for gastrin and CCK (36).…”

Section: Discussionmentioning

confidence: 99%

Gastrin receptors on isolated canine parietal cells.

Soll¹,

Amirian²,

Thomas³

et al. 1984

J. Clin. Invest.

222

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Section: Discussionmentioning

confidence: 99%

Gastrin receptors on isolated canine parietal cells.

Soll¹,

Amirian²,

Thomas³

et al. 1984

J. Clin. Invest.

222

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“…Although existing in a range of molecular forms (Rehfetd 1992), the vast bulk of neuronal CCK comprises the sulphated octapeptide, CCK-8s (Sauter and Frick 1983), while the C-terminus tetrapeptide amide (Trp-Met-Asp-Phe-NH2) appears to be the minimum requirement for biological activity (Rehfeld 1992). CCK interacts with at least two receptor subtypes (Hays et al 1980;Innis and Snyder 1980;Jensen et al 1980;Saito et al 1980), now referred to as CCKA and CCKB receptors (Moran et al 1986). Although CCK has been implicated in a range of physiological and behavioural functions (for recent review, see Crawley and Corwin 1994), the past 5 years have witnessed considerable interest in its potential involvement in the mechanisms of anxiety (for review, see Harro and Vasar 1991a;Bradwejn et al 1992;Harro et al 1993;Rodgers and Johnson 1995a).…”

Section: Introductionmentioning

confidence: 99%

Ethological analysis of cholecystokinin (CCKA and CCKB) receptor ligands in the elevated plus-maze test of anxiety in mice

Johnson

Rodgers

1996

Psychopharmacology

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The literature on the effects of CCK receptor manipulations in animal models of anxiety is rife with inconsistency, and the data subject to a variety of methodological and interpretative difficulties. In the present paper, the effects of a range of CCK receptor ligands on anxiety in male mice have been assessed using an ethological version of the elevated plus-maze test. Compounds selected for study were the agonists, CCK-4 and CCK-8s (12.5-100 micrograms/kg), and the antagonists, devazepide, L-365, 260 and PD 135158 (1.0 microgram/kg-1.0 mg/kg). CCK-4 failed to produce any significant behavioural effects over the dose range tested, while treatment with the sulphated octapeptide, CCK-8s, induced signs of behavioural inhibition at 100 microgram/kg without altering anxiety-related indices. Furthermore, in contrast to the clear anxiolytic profile of diazepam (1 mg/kg), and despite the comprehensive behavioural profiles yielded by ethological analysis, all three CCK receptor antagonists studied (devazepide, L-365, 260 and PD 135158) were found to be without significant effect under present test conditions. Together, present findings provide little support for the involvement of CCK receptor mechanisms in anxiety and, in particular, the form of anxiety evoked in mice by exposure to a plus-maze.

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“…To date, two CCK receptors have been distinguished (designated CCK A and CCK B ) based on their molecular characterization and different pharmacological profiles. Both receptors couple to G-proteins (Wank et al, 1994), and their relative distributions in the CNS and peripheral nervous system correlate well with CCK immunoreactivity (Dockray, 1987;Hays et al, 1980;Innis and Snyder, 1980). Cholecystokinin receptors have been shown to interact with several different cellular transduction systems in central and peripheral tissues, including the activation of phospholipase C (Kuwahara et al, 1993;Lee et al, 1993;Wu and Wang, 1996b), the modulation of potassium and calcium channels (Boden and Hill, 1988;Buckett and Saint, 1989;Miyoshi et al, 1991;Branchereau et al, 1993;Cox et al, 1995;Liu et al, 1995), and activation of nonselective cation channels (Dodd and Kelly, 1981;Jarvis et al, 1992).…”

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confidence: 99%

Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons

Miller¹,

Hoffer²,

Svoboda³

et al. 1997

J. Neurosci.

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Cholecystokinin (CCK) is found co-localized with the inhibitory neurotransmitter GABA in interneurons of the hippocampus. Also, CCK receptors are found in abundance in this brain region. The possibility that CCK alters interneuron activity was examined using whole-cell current-and voltage-clamp recordings from visualized interneurons in the stratum radiatum of area CA1 in rat hippocampal slices. The effect of CCK on GABA-mediated IPSCs was also determined in pyramidal neurons. The sulfated octapeptide CCK-8S increased action potential frequency or generated inward currents in the majority of interneurons. These effects of CCK persisted in the presence of tetrodotoxin and cadmium, suggesting that they were direct. Current-voltage plots revealed that CCK-8S inhibited a conductance that was linear across command potentials and reversed near the equilibrium potential for K ϩ ions. The K ϩ channel blocker tetraethylammonium (10 mM) generated inward currents similar to those initiated by CCK, and it occluded the effect of the peptide. BaCl 2 (1 mM) and 4-aminopyridine (2 mM) did not alter the effect of CCK. The CCK B receptor antagonist PD-135,158 completely blocked the inward currents generated by CCK-8S. CCK also resulted in an increase in spontaneous action potential-dependent IPSC frequency, but no changes in action potential-independent miniature IPSCs or evoked IPSCs in pyramidal neurons. These results provide evidence that CCK can depolarize hippocampal interneurons through the inhibition of a resting K ϩ conductance, leading to increased tonic inhibition of pyramidal neurons. This action of CCK may contribute to its anticonvulsant properties, as observed in limbic seizure models.

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Demonstration of a putative receptor site for cholecystokinin in rat brain

Cited by 177 publications

References 15 publications

Gastrin receptors on isolated canine parietal cells.

Gastrin receptors on isolated canine parietal cells.

Ethological analysis of cholecystokinin (CCKA and CCKB) receptor ligands in the elevated plus-maze test of anxiety in mice

Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons

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Demonstration of a putative receptor site for cholecystokinin in rat brain

Cited by 177 publications

References 15 publications

Gastrin receptors on isolated canine parietal cells.

Gastrin receptors on isolated canine parietal cells.

Ethological analysis of cholecystokinin (CCKA and CCKB) receptor ligands in the elevated plus-maze test of anxiety in mice

Cholecystokinin Increases GABA Release by Inhibiting a Resting K+Conductance in Hippocampal Interneurons

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Cholecystokinin Increases GABA Release by Inhibiting a Resting K⁺Conductance in Hippocampal Interneurons