L-364,718, a cholecystokinin-A receptor antagonist, suppresses feeding-induced sleep in rats

Shemyakin, Alexei; Kapás, Levente

doi:10.1152/ajpregu.2001.280.5.r1420

Cited by 28 publications

(13 citation statements)

References 31 publications

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“…Thus, the activation of CCK to activate orexin neurons appears paradoxical because CCK suppresses food intake (Gibbs et al, 1973;Schick et al, 1986;Kopin et al, 1999) and locomotor activity (Hirosue et al, 1992) when administered intraperitoneally or intracerebroventricularly. It has also been reported that a CCK A R antagonist, L-364,718, suppresses feeding-induced sleep in rats, suggesting that CCK A R activation might participate in postprandial hypersomnolence and that CCK is a somnogen (Shemyakin and Kapas, 2001).…”

Section: Physiological Significance Of Cck-8s-mediated Activation Of mentioning

confidence: 97%

Cholecystokinin Activates Orexin/Hypocretin Neurons through the Cholecystokinin A Receptor

Tsujino¹,

Yamanaka²,

Ichiki³

et al. 2005

J. Neurosci.

132

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Orexin A and B are neuropeptides implicated in the regulation of sleep/wakefulness and energy homeostasis. The regulatory mechanism of the activity of orexin neurons is not precisely understood. Using transgenic mice in which orexin neurons specifically express yellow cameleon 2.1, we screened for factors that affect the activity of orexin neurons (a total of 21 peptides and six other factors were examined) and found that a sulfated octapeptide form of cholecystokinin (CCK-8S), neurotensin, oxytocin, and vasopressin activate orexin neurons. The mechanisms that underlie CCK-8S-induced activation of orexin neurons were studied by both calcium imaging and slice patch-clamp recording. CCK-8S induced inward current in the orexin neurons. The CCK A receptor antagonist lorglumide inhibited CCK-8S-induced activation of orexin neurons, whereas the CCK B receptor agonists CCK-4 (a tetrapeptide form of cholecystokinin) and nonsulfated CCK-8 had little effect. The CCK-8S-induced increase in intracellular calcium concentration was eliminated by removing extracellular calcium but not by an addition of thapsigargin. Nifedipine, -conotoxin, -agatoxin, 4-ethylphenylamino-1,2-dimethyl-6-methylaminopyrimidinium chloride, and SNX-482 had little effect, but La 3ϩ , Gd 3ϩ , and 2-aminoethoxydiphenylborate inhibited CCK-8S-induced calcium influx. Additionally, the CCK-8S-induced inward current was dramatically enhanced in the calcium-free solution and was inhibited by the cation channel blocker SKF96365, suggesting an involvement of extracellular calcium-sensitive cation channels. CCK-8S did not induce an increase in intracellular calcium concentration when membrane potential was clamped at Ϫ60 mV, suggesting that the calcium increase is induced by depolarization. The evidence presented here expands our understanding of the regulation of orexin neurons and the physiological role of CCK in the CNS.

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Section: Physiological Significance Of Cck-8s-mediated Activation Of mentioning

confidence: 97%

Cholecystokinin Activates Orexin/Hypocretin Neurons through the Cholecystokinin A Receptor

Tsujino¹,

Yamanaka²,

Ichiki³

et al. 2005

J. Neurosci.

132

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“…These sleep-loss effects develop more rapidly if the initial energy levels of the body are low (3,10). In contrast, refeeding after food deprivation increases sleep in rats (3,33). Rats kept on a calorie-rich "cafeteria diet" tend to overeat and have an increased amount of sleep (7,15).…”

mentioning

confidence: 99%

Restricted feeding-induced sleep, activity, and body temperature changes in normal and preproghrelin-deficient mice

Szentirmai

Kapás

Sun

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Behavioral and physiological rhythms can be entrained by daily restricted feeding (RF), indicating the existence of a food-entrainable oscillator (FEO). One manifestation of the presence of FEO is anticipatory activity to regularly scheduled feeding. In the present study, we tested if intact ghrelin signaling is required for FEO function by studying food anticipatory activity (FAA) in preproghrelin knockout (KO) and wild-type (WT) mice. Sleep-wake activity, locomotor activity, body temperature, food intake, and body weight were measured for 12 days in mice on a RF paradigm with food available only for 4 h daily during the light phase. On RF days 1-3, increases in arousal occurred. This response was significantly attenuated in preproghrelin KO mice. There were progressive changes in sleep architecture and body temperature during the subsequent nine RF days. Sleep increased at night and decreased during the light periods while the total daily amount of sleep remained at baseline levels in both KO and WT mice. Body temperature fell during the dark but was elevated during and after feeding in the light. In the premeal hours, anticipatory increases in body temperature, locomotor activity, and wakefulness were present from RF day 6 in both groups. Results indicate that the preproghrelin gene is not required for the manifestation of FAA but suggest a role for ghrelinergic mechanisms in food deprivation-induced arousal in mice.

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“…Furthermore, postprandial sleep has been linked to the satiety-promoting hormone, cholecystokinin (CCK; Shemyakin and Kapas, 2001). However in humans, sleep changes in response to a meal are highly variable (Stahl et al, 1983).…”

Section: Discussionmentioning

confidence: 99%

Increased food intake after starvation enhances sleep in Drosophila melanogaster

Regalado

Cortez

Grubbs

et al. 2017

Journal of Genetics and Genomics

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Feeding and sleep are highly conserved, interconnected behaviors essential for survival. Starvation has been shown to potently suppress sleep across species; however, whether satiety promotes sleep is still unclear. Here we use the fruit fly, Drosophila melanogaster, as a model organism to address the interactions between feeding and sleep. We first monitored the sleep of flies that had been starved for 24 h and found that sleep amount increased in the first 4 h after flies were given food. Increased sleep after starvation was due to an increase in sleep bout number and average sleep bout length. Mutants of translin or adipokinetic hormone, which fail to suppress sleep during starvation, still exhibited a sleep increase after starvation, suggesting that sleep increase after starvation is not a consequence of sleep loss during starvation. We also found that feeding activity and food consumption were higher in the first 10‒30 min after starvation. Restricting food consumption in starved flies to 30 min was sufficient to increase sleep for 1 h. Although flies ingested a comparable amount of food at differing sucrose concentrations, sleep increase after starvation on a lower sucrose concentration was undetectable. Taken together, our results suggest increased food intake after starvation enhances sleep and reveals a novel relationship between feeding and sleep.

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L-364,718, a cholecystokinin-A receptor antagonist, suppresses feeding-induced sleep in rats

Cited by 28 publications

References 31 publications

Cholecystokinin Activates Orexin/Hypocretin Neurons through the Cholecystokinin A Receptor

Cholecystokinin Activates Orexin/Hypocretin Neurons through the Cholecystokinin A Receptor

Restricted feeding-induced sleep, activity, and body temperature changes in normal and preproghrelin-deficient mice

Increased food intake after starvation enhances sleep in Drosophila melanogaster

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