Modulation of Memory Processing by Cholecystokinin: Dependence on the Vagus Nerve

Flood, James F.; Smith, G. Troy; Morley, John E.

doi:10.1126/science.3576201

Cited by 180 publications

(68 citation statements)

References 13 publications

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“…Stimulation of the vagus nerve results in increased electrical activity in the central nucleus of the amygdala and in the hippocampus (12,51). Previous studies indicate that systemically administered CCK facilitates memory performance via CCK1 receptors located on vagal afferent nerves (14,19,20,60,15). Vagal fibers enter the hindbrain at the level of NTS, and CCK1 receptors are abundant in the area postrema and NTS (25,28,67).…”

Section: Discussionmentioning

confidence: 99%

Characterization of mice lacking the gene for cholecystokinin

Samuelson²,

Chambers

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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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 watermaze 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. cholecystokinin 1 receptor; cholecystokinin 2 receptor; cognitive behaviors CCK OCCURS as a carboxyl terminally amidated peptide that exists in several possible lengths (43,58,66). In rats and mice, the predominant circulating forms include cholecystokinin octapeptide (CCK-8) and CCK-22, whereas larger molecular forms (CCK-33 and CCK-58) are also present in human and canine plasma (42,61,38,63,16). These molecular forms are processed from a 115-amino acid preprohormone product of the gene residing in chromosome 3 in rodents (13, 57). Intestinal endocrine cells secrete a mixture of medium-sized CCK forms, while central and peripheral neurons mainly release sulfated forms of 62). In response to consumption of either lipid and protein, CCK is produced and secreted by intestinal I cells (41). The release of CCK from neurons is caused by potassium ion-induced depolarization (15). Peripheral CCK is involved in modulating intestinal motility, stimulating pancreatic enzyme secretion, enhancing gallbladder contraction, and regulating meal size (11,21,24,29,48,56,64,69).CCK is also a neurotransmitter in many areas of the nervous system (6). Intraperitoneal or central administration of either purified CCK extracts or synthetic CCK-8 to fasted rats reduces food intake (22,33,37,54), and this is manifested by a reduction of meal size as opposed to reduced frequency of meals (22,37). Two types of CCK receptors (CCK1...

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Section: Discussionmentioning

confidence: 99%

Characterization of mice lacking the gene for cholecystokinin

Samuelson²,

Chambers

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Other peripherally acting agents that conduct ascending information through the vagus nerve demonstrate a similar inverted-U response [4,5,[135][136][137][138]. The precise mechanisms that underlie this response profile are not understood, but several explanations could account for the inverted-U response.…”

Section: Optimizing Vns Parametersmentioning

confidence: 99%

“…In rodents, behavioral training immediately followed by administration of a variety of peripherally acting agents that do not readily cross the blood-brain barrier, including cholecystokinin, bombesin, gastrinreleasing peptide, 4-OH amphetamine, substance P, and Lglucose, improved consolidation of memory [4][5][6][7][8][9]. Vagotomy blocked the memory enhancing effects of these chemical stimuli, suggesting that the ascending projections of the vagus may act as a conduit to relay peripheral information to the central nervous system (CNS) [4][5][6][7][8][9]. If chemical stimulation with these agents activates fibers of the vagus nerve to enhance memory, then electrical stimulation of the nerve would be expected to have a similar effect.…”

Section: Introductionmentioning

confidence: 99%

Enhancing Rehabilitative Therapies with Vagus Nerve Stimulation

Hays

2016

Neurotherapeutics

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Pathological neural activity could be treated by directing specific plasticity to renormalize circuits and restore function. Rehabilitative therapies aim to promote adaptive circuit changes after neurological disease or injury, but insufficient or maladaptive plasticity often prevents a full recovery. The development of adjunctive strategies that broadly support plasticity to facilitate the benefits of rehabilitative interventions has the potential to improve treatment of a wide range of neurological disorders. Recently, stimulation of the vagus nerve in conjunction with rehabilitation has emerged as one such potential targeted plasticity therapy. Vagus nerve stimulation (VNS) drives activation of neuromodulatory nuclei that are associated with plasticity, including the cholinergic basal forebrain and the noradrenergic locus coeruleus. Repeatedly pairing brief bursts of VNS sensory or motor events drives robust, event-specific plasticity in neural circuits. Animal models of chronic tinnitus, ischemic stroke, intracerebral hemorrhage, traumatic brain injury, and post-traumatic stress disorder benefit from delivery of VNS paired with successful trials during rehabilitative training. Moreover, mounting evidence from pilot clinical trials provides an initial indication that VNS-based targeted plasticity therapies may be effective in patients with neurological diseases and injuries. Here, I provide a discussion of the current uses and potential future applications of VNS-based targeted plasticity therapies in animal models and patients, and outline challenges for clinical implementation.

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“…This gastrointestinal hormone appears to produce its effect on memory by activating ascending vagal fibers. A link may have evolved between the release of gastric peptides and memory processing in the central nervous system because of the survival advantages conferred to an animal that remembers the details of a successful food-foraging expedition (Flood, Smith, & Morley, 1987). Feeding is important for mothers to promote the lactation process, and a link between memory and feeding could be established by studying the role of the CCK hormone in maternal memory and how it can improve the lactation process and development of the offspring.…”

Section: Future Directions: Cck Cognition and Maternal Behaviormentioning

confidence: 99%

Cholecystokinin Modulation of Maternal Behavior.

Felício¹,

Cruz²,

Schroêder³

et al. 2013

Psychology & Neuroscience

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Maternal behavior is regulated by several neurotransmitters, neuropeptides, and hormones. This mini-review focuses on the role of cholecystokinin (CCK), a neuropeptide and gut hormone best known as a satiety signal, in mediating maternal behavior. In addition to the role of CCK in the infant in mother-infant interactions, maternal CCK appears to also be important. We discuss maternal behavior research, mainly in rats, that has examined the effect of administering CCK to dams, CCK-opioid interactions, and maternal behavior in rats that lack CCK1 receptors. We discuss the possibility that CCK might play a role in neurological adjustments during pregnancy that ultimately influence behavioral adaptations by the offspring during lactation. Finally, we hypothesize that maternal CCK is also involved in maternal memory and reward.

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Modulation of Memory Processing by Cholecystokinin: Dependence on the Vagus Nerve

Cited by 180 publications

References 13 publications

Characterization of mice lacking the gene for cholecystokinin

Characterization of mice lacking the gene for cholecystokinin

Enhancing Rehabilitative Therapies with Vagus Nerve Stimulation

Cholecystokinin Modulation of Maternal Behavior.

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