Acute effect of cholecystokinin on short-term synaptic plasticity in the rat hippocampus.

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Abstract

Cholecystokinin (CCK), a peptide hormone found in the gut, is the most abundant peptide neurotransmitters in the brain, and its acute effects on the brain activity have been shown. In this study we aimed to evaluate the acute effects of CCK on short-term synaptic plasticity in the dentate gyrus (DG) of the rat hippocampus. Via stereotaxic surgery, the stimulating and the recording electrodes were placed in the perforant pathway and dentate gyrus, respectively and 30 min after intraperitoneal (i.p.) injection of CCK octapeptide sulfated (CCK-8S, 1.6 μg/kg), evoked responses were recorded after delivering of paired-pulse stimulations at 10 to 500 ms inter-stimulus intervals. With respect to the control group that received saline instead of CCK, in baseline responses, slope of field excitatory postsynaptic potential (fEPSP) 5 min and 10 min after injection of CCK-8S (p<0.05) and population spikes (PS)- amplitudes 5 min after injection of CCK-8S (p<0.05) were significantly increased. In paired pulse responses, PS amplitudes were increased in the CCK group, but these enhancements only were significant at inter-stimulus interval 40 ms (p<0.05). However fEPSP slopes were decreased at inter-stimulus intervals 70 ms (p<0.05), 120 ms (p<0.01), 150 ms (p<0.001) and 300 ms (p<0.001). The results showed that CCK-8S has a transient excitatory effects on baseline responses, but it inhibits paired pulse indices in acute. Therefore, in a short period of time, effect of CCK on the function of synapses is time dependent, and it has stimulatory or inhibitory effects at different time periods.

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Cell type-specific gating of perisomatic inhibition by cholecystokinin.

Janos Szabadics, Axel Neu, Ivan Soltesz … (2007)

Parvalbumin- and cholecystokinin (CCK)-expressing basket cells provide two parallel, functionally distinct sources of perisomatic inhibition to postsynaptic cells. We show that exogenously applied CCK enhances the output from rat parvalbumin-expressing basket cells, while concurrently suppressing GABA release from CCK-expressing neurons through retrograde endocannabinoid action. These results indicate that CCK may act as a molecular switch that determines the source of perisomatic inhibition for hippocampal principal cells.

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Characterization of mice lacking the gene for cholecystokinin.

Chun-Hsien Lo, J. Chambers, Linda Samuelson … (2008)

CCK acts peripherally as a satiating peptide released during meals in response to lipid feeding and centrally functions in the modulation of feeding, exploratory, and memory activities. The present study determined metabolic parameters, food intake, anxiety-like behaviors, and cognitive function in mice lacking the CCK gene. We studied intestinal fat absorption, body composition, and food intake of CCK knockout (CCK-KO) mice by using the noninvasive measurement of intestinal fat absorption along with quantitative magnetic resonance (QMR) imaging and the DietMax system, respectively. Additionally, exploratory and memory capacities were assessed by monitoring running wheel activity and conducting elevated plus-maze and Morris water-maze tests with these mice. Compared with wild-type (WT) littermate controls, CCK-KO mice had normal food intake, fat absorption, body weight, and body mass. CCK-KO mice ate more food than control animals during the light period and less food during the dark period. Energy expenditure was unchanged between the genotypes; however, CCK-KO mice displayed greater fatty acid oxidation. CCK-KO mice were as active as WT animals in the running wheel test. CCK-KO mice spent more time in the closed arms of an elevated plus-maze, indicative of increased anxiety. Additionally, CCK-KO mice exhibited attenuated performance in a passive avoidance task and impaired spatial memory in the Morris water maze test. We conclude that CCK is involved in metabolic rate and is important for memory and exploration. CCK is intimately involved in multiple processes related to cognitive function and food intake regulation.

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Cholecystokinin facilitates glutamate release by increasing the number of readily releasable vesicles and releasing probability.

J. Porter, Tony Xiao, Pan Deng … (2010)

Cholecystokinin (CCK), a neuropeptide originally discovered in the gastrointestinal tract, is abundantly distributed in the mammalian brains including the hippocampus. Whereas CCK has been shown to increase glutamate concentration in the perfusate of hippocampal slices and in purified rat hippocampal synaptosomes, the cellular and molecular mechanisms whereby CCK modulates glutamatergic function remain unexplored. Here, we examined the effects of CCK on glutamatergic transmission in the hippocampus using whole-cell recordings from hippocampal slices. Application of CCK increased AMPA receptor-mediated EPSCs at perforant path-dentate gyrus granule cell, CA3-CA3 and Schaffer collateral-CA1 synapses without effects at mossy fiber-CA3 synapses. CCK-induced increases in AMPA EPSCs were mediated by CCK-2 receptors and were not modulated developmentally and transcriptionally. CCK reduced the coefficient of variation and paired-pulse ratio of AMPA EPSCs suggesting that CCK facilitates presynaptic glutamate release. CCK increased the release probability and the number of readily releasable vesicles with no effects on the rate of recovery from vesicle depletion. CCK-mediated increases in glutamate release required the functions of phospholipase C, intracellular Ca(2+) release and protein kinase Cgamma. CCK released endogenously from hippocampal interneurons facilitated glutamatergic transmission. Our results provide a cellular and molecular mechanism to explain the roles of CCK in the brain.