Effects of Cholecystokinin Tetra and Octa Peptides on Locomotor Activity in Mice

Takeda, Yasuo; Takáno, Yukio; Kamiya, Hiro-o

doi:10.1254/jjp.42.145

Cited by 6 publications

(4 citation statements)

References 19 publications

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“…Our finding that CCK-4 had relatively high ability to bind to the CCK receptor in the cerebral cortex is consistent with these re ports. The present results for CCK-4 in dis placement experiments also support our previous finding that intraperitoneal injection of CCK-4 as well as of CCK-8 suppressed locomotor hyperactivity induced by metham phetamine and TRH in mice (6).…”

Section: Discussionsupporting

confidence: 92%

Comparison of CCK-8 receptors in the pancreas and brain of rats using CCK-8 analogues.

et al. 1989

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Abstract-The characteristics of cholecystokinin (CCK) receptors in rat pancreatic acini and in various regions of the brain were examined using synthetic CCK-8 or CCK-7 analogues. 3H-propionylated CCK-8 ([3H] This order of potencies of CCK analogues was greatly different from that in the cerebral cortex.3) The carboxy-terminal tetra-peptide (CCK-4) and penta-peptide (CCK-5) had very weak potencies in displacing [3H]CCK-8 binding in the pancreatic acini, which were 20 to 30-fold less than their potencies in the cerebral cortex. These results suggest that the recognition sites for CCK analogues in the pancreatic and brain CCK receptors are different.

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Section: Discussionsupporting

confidence: 92%

Comparison of CCK-8 receptors in the pancreas and brain of rats using CCK-8 analogues.

et al. 1989

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“…Cholecystokinin (CCK) is a peptide synthesised throughout the gastrointestinal tract that also acts on the brain to decrease appetite (78). CCK has also been found to decrease locomotion when given both centrally and systemically (79–82). More specifically, CCK induces a ‘satiety sequence’ that includes decreased locomotor activity and rearing (81).…”

Section: Sensorsmentioning

confidence: 99%

“…First, CCK does not fit the usual pattern of satiety signals of increasing NEAT. Through its actions on the NTS, CCK initiates a behavioural satiety sequence that includes decreased locomotor activity, probably through activation of CCK‐A receptors that affect dopaminergic mechanisms (78, 79, 81, 84, 189). The vagus nerve is also important in mediating the ability of CCK to induce satiety (190).…”

Section: Integration Of Energy Balance Signalsmentioning

confidence: 99%

Central Neural and Endocrine Mechanisms of Non‐Exercise Activity Thermogenesis and Their Potential Impact on Obesity

Novak

Levine

2007

J Neuroendocrinology

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Obesity is an ever-increasing problem now that more than one billion people worldwide are overweight or obese (1). More than one-half of Americans are overweight, and the proportion of the population that is overweight, obese, or extremely obese continues to grow (2, 3). Developing nations are quickly catching up with more developed countries with respect to rates of obesity and related health problems (4). This trend cuts across ethnicity, age, gender, and education level (5, 6). Childhood obesity, which portends adult obesity and predicts health problems in adulthood (7), continues to increase (8). Obesity is associated with a slew of deleterious health effects and health-related risk factors, including diabetes, cardiovascular disease, high cholesterol, asthma, arthritis, sleep apnoea, and cancer (6, 9-13), and is also linked with decreased life span (14), disability (15), and a lower in quality of life (16).Weight gain results when energy expenditure is inappropriately low for the caloric intake of an individual. The role of dietary intake and its underlying mechanisms have been the principal focus when examining the rise in obesity (17, 18). Obesity incidence has risen, however, even as dietary quality has improved or energy intake has been reduced (17,18). This circumstance necessitates a critical examination of the other side of the energy balance equation, namely energy expenditure. As illustrated in Fig. 1, total daily energy expenditure (TDEE) consists of basal metabolic rate (BMR), the thermic effect of food, and the energy expenditure of activity. Some studies find a decreased BMR in those predisposed to become obese (19)(20)(21). Even in these obesity-prone individuals, however, the decrease in BMR could not fully explain the positive energy balance incurred (19), and the energy expenditure of physical activity was directly implicated in the development of obesity (20). Smaller, tightly controlled studies lend little support to the belief that differences in resting energy expenditure contribute to the tendency of an individual to gain weight (22, 23). Next, the thermic effect of food contributes little to TDEE in terms of both absolute kcal ⁄ day and variability. This suggests that the remaining component of TDEE is likely to change with obesity and the propensity to gain weight, specifically the energy expenditure of activity. At the population level, sedentary behaviour has increased steadily as physical activity has decreased, and this corresponds to increased obesity and decreased health in both children and adults (22,(24)(25)(26)(27)(28). The current trend in the general population is opposed to communities with heavy physical activity demands, which show very low rates of obesity (29). Indeed, increasing physical activity levels may be the missing link needed to reverse the current obesity trends (18,22,24,25,27,30). The rise in obesity is associated with a decline in the amount of physical activity in which people engage. The energy expended through everyday non-exercise activity, called no...

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“…The nonsulfated octapeptide ccK,Ns and the C-terminal fragment CCK4 could be used as CCKB agonists since in the guinea pig, they have 100 to 1,000 times lower affinity than CCK, for peripheral binding sites but only an -10-fold smaller affinity for central receptors (Innis and Snyder, 1980;Saito et al, 1980). However, these two compounds were shown to be ineffective in several pharmacological experimente in apparent contradiction with results ofbinding studies (review in Crawley, 1988;De Witte et al, 1987;Hsiao et al, 1984;Katsuura et al, 1985;Morin et al, 1983;Moroji and Hagino, 1986;Schneider et al, 1983;Takeda et al, 1986;Worms et al, 1986). Recently, a new CCK analog, Boc-Tyr (S0,H)-gNle-mGly-Trp-(NMe)-Nle-Asp-PheNH, (BC 264) endowed with high affinity and selectivity for CCKB receptors in guinea pig has been synthesized.…”

Section: Introductionmentioning

confidence: 99%

Investigation of behavioral and electrophysiological responses induced by selective stimulation of CCKB receptors by using a new highly potent CCK analog, BC 264

Dauge

Böhme

Crawley

et al. 1990

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The new CCKB analog, Boc-Tyr (SO3H)-gNle-mGly-Trp-(NMe)-Nle-Asp-PheNH2 (BC 264) exhibited a high affinity (KI = 0.39 +/- 0.15 nM) and selectivity for central (B) versus peripheral (A) receptors (KI CCKA/KI CCKB = 910) in the rat. In agreement with these binding studies, BC 264 was at least 50 times more potent than CCK8 in stimulating the firing of rat CA hippocampal neurones. Furthermore stereotaxic injection of BC 264 or CCK8 in the VTA of rats resulted in potentiation of the dopamine-induced hypolocomotion. These two types of CCK8 responses have been previously shown in involve CCKB receptors. In contrast, after administration into the postero-median nucleus accumbens, the hypoexploration, the increase of emotionality of rats, or the potentiation of dopamine-induced hyperlocomotion were obtained after injection of CCK8 but not of BC 264, supporting the involvement of peripheral CCKA receptors in these CCK8 responses. Owing to its resistance to peptidases, BC 264 appears to be of great interest in the investigation of the still uncertain functional roles of CCK in the central nervous system.

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Effects of Cholecystokinin Tetra and Octa Peptides on Locomotor Activity in Mice

Cited by 6 publications

References 19 publications

Comparison of CCK-8 receptors in the pancreas and brain of rats using CCK-8 analogues.

Comparison of CCK-8 receptors in the pancreas and brain of rats using CCK-8 analogues.

Central Neural and Endocrine Mechanisms of Non‐Exercise Activity Thermogenesis and Their Potential Impact on Obesity

Investigation of behavioral and electrophysiological responses induced by selective stimulation of CCKB receptors by using a new highly potent CCK analog, BC 264

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