Inhibition of feeding by the C-terminal tetrapeptide fragment of cholecystokinin in a novel environment (original) (raw)
Related papers
1985
The effects of cholecystokinin octapeptide sulfate ester (CCK-8-SE) and nonsulfated cholecystokinin octapeptide (CCK-8-NS) were tested on feeding by rats in familiar and novel environment. In a familiar environment only intraperitoneally (IP) administered CCK-8-SE (0.8-24 nmole/kg) could inhibit 30 min food intake of 24 hr food-deprived rats, while the same doses of CCK-8-NS IP and both octapeptides (0.8-8000 pmole/rat) intracerebroventricularly (ICV) were totally ineffective. The effects of CCK-8-SE and CCK-8-NS on feeding were also tested in a novel environment, i.e., in an open field. The parameters of exploratory activity and food intake of 24-hr food-deprived rats were recorded simultaneously during a 15-min session. After IP injection, CCK-8-SE dose-dependently depressed the food intake, and the higher doses (8.0 or 24 nmole/kg) also decreased the open field parameters, including number of approaches to food. In the novel environment, 8.0 or 24 nmole/kg IP injected CCK-8-NS al...
Changes in the satiating effect of cholecystokinin over repeated trials
The study investigated the reasons for discrepant published results concerning a diminution of the satiating action of cholecystokinin (CCK) when it is administered over several trials. Throughout the experiment, rats were maintained on a schedule in which they were fasted for 5.5 h (except 5 ml of milk), and then given access to a 10% sucrose solution for 30 min. Following a baseline period, rats received 6 Ag/kg CCK-8 every day (consecutive group) or every third day (intermittent group), or saline (saline group), 15 min prior to the sucrose. In the consecutive group, CCK-8 significantly reduced meal size on day 1 (85.1 T 7.4% of baseline) compared to the saline group (106.9 T 7.5% of baseline), p < 0.05. This reduction was eliminated by day 5 (consecutive group = 94.9 T 4.7% of baseline, saline group = 98.0 T 5.2% of baseline). In contrast, the intermittent group never became insensitive to the effect of CCK-8, reducing their intake comparably after the tenth (intermittent group = 138.7 T 8.2% of baseline, saline group = 176.0 T 9.1% of baseline, p < 0.01), and first CCK-8 injection (intermittent group = 77.0 T 6.1% of baseline, saline group = 106.9 T 7.5% of baseline, p < 0.01). Although it has been hypothesized that this phenomenon is due to behavioral tolerance, the results of this experiment suggest an alternate hypothesis; i.e., that the diminution of the effect of CCK-8 over consecutive administrations is due to the extinction of a previously learned response to endogenous CCK. D
Species Differences in the Response to Cholecystokinin
Annals of the New York Academy of Sciences, 1985
Cholecystokinin (CCK), one of the classical gastrointestinal hormones, also appears to be important as a putative neurotransmitter.' With the exponential increase in the number of studies on the effects of CCK on behavior, it has become clear that marked species differences in responsiveness exist. The failure to acknowledge this has led to a number of disputes in the literature. In this brief communication we will review the evidence for differing responses to the inhibition of feeding by CCK in a number of different species.
Effects of cholecystokinin-related peptides on self-stimulation behaviour in rats
Neuropeptides, 1988
The effects of cholecystokinin octapeptide sulfate ester (CCK-&SE), its N-terminal tripeptide (CCK-2-4-SE) and its C-terminal tetrapeptide (CCK-5-8) were investigated on hypothalamic self-stimulation in rats. CCK-&SE and CCK-5-8 in 400 pmole doses inhibited self-stimulation behaviour, while CCK-2-4-SE was ineffective. In 80 pmole doses the peptides showed no effect. It is suggested that CCK-5-8 itself influences self-stimulation behaviour.
Experimental physiology, 1991
The effects on vasopressin and cortisol secretion of centrally and peripherally administered cholecystokinin octapeptide (CCK) were investigated in conscious prepubertal pigs. Injection of 1.3 micrograms CCK into the lateral cerebral ventricle resulted in a sustained increase in plasma vasopressin after a latency of 5 min but no change in cortisol concentrations. Intravenous injection of 0.7 and 1.3 micrograms/kg CCK initiated a rapid surge (within 2 min) in plasma vasopressin and a later increase in cortisol secretion. The time course of the vasopressin response to the central injection of CCK was found to be similar to the period of behavioural inhibition induced when an equivalent dose of the peptide was given by the same route in an earlier feeding experiment. An analogous situation was also observed when CCK was given peripherally and, in this case, the threshold dose at which the behavioural and endocrine responses were induced was found to be the same.
Cholecystokinin decreases food intake in rats
Journal of Comparative and Physiological Psychology, 1973
Partially purified cholecystokinin (CCK) was injected intraperitoneally into fasted rats prior to food presentation. The hormone produced a large dose-related suppression of intake of solid and liquid diets. Identical doses of the synthetic terminal octapeptide of cholecystokinin produced identical results. An effective dose of CCK did not suppress drinking after water deprivation. Treated animals did not appear ill and were not hyperthermic; neither CCK nor the octapeptide produced learning of a taste aversion in bait-shyness tests. The effect of CCK is not a property of all gut hormones, since injections of secretin did not affect feeding. These studies raise the possibility that CCK plays an inhibitory role in the short-term control of feeding behavior.
The neuropharmacology and behavioural effects of cholecystokinin
2005
Cholecystokinin Receptor Distribution CCK-binding sites were first described in the brain in the early nineteen-eighties (Hays et al., 1980; Innis and Snyder, 1980; Saito et al., 1980). Various studies using autoradiography, insitu hybridisation and immunocytochemistry have investigated regional distribution using nonselective cholecystokinin specific ligands in numerous species. These studies demonstrated that despite similarities, there are also marked variations in the comparative distribution between species. CCK 1 receptors are located in the pancreatic acini, gastric mucosa, gallbladder, gastrointestinal tract and specific areas of the central nervous system. Rat CCK 1 receptors are located in the interpeduncular nucleus (Hill et al., 1988), area postrema, and medial nucleus tractus solitarius, with additional areas of binding found in the habenular nuclei, dorsomedial nucleus of the hypothalamus, and central amygdala (
Cholecystokinin reduces exploratory behavior in mice
Physiology & behavior, 1981
reduces exploratory behavior in mice. PHYSIOL. BEHAV. 27(3) [407][408][409][410][411] 1981.--The role of cholecystokinin (CCK) in mediating spontaneous behaviors in mice was analyzed, using a video-tracking, computer-assisted animal behavior monitoring system. Intraperitoneal administration of cholecystokinin octapeptide decreased investigation of environmental objects and interactions with a female mouse, while increasing the amount of time spent in the comers of the test arena and the duration of nonexploratory pauses. Dose-dependent effects were seen in the range of 0.12-50 #g/kg. Other parameters of motor activity were normal, indicating that the reduction in exploratory tendencies is not a function of sedation or loss of motor coordination. Neither gastrin nor unsulfated cholecystokininx changed any of the measured parameters, indicating pharmacological specificity for the observed reduction in exploration.