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1.
The role of Cholecystokinin in the hyperphagia of lactation was studied by measuring the concentration of this hormone in plasma and cerebrospinal fluid in relation to food intake in lactating rats. Cholecystokinin was measured by high-performance liquid chromatography and radioimmunoassay in plasma and by radioimmunoassay in cerebrospinal fluid. Plasma concentrations of Cholecystokinin were increased in freely-fed lactating rats compared with non-lactating, regularly cycling rats. However, after 24 h of food deprivation the concentration of plasma Cholecystokinin was markedly decreased in the lactating rats to levels which were lower than those of non-lactating animals. Furthermore, plasma levels of Cholecystokinin did not increase in response to 1 h of feeding in lactating rats, whereas in non-lactating rats they did. In contrast, the concentration of cholecystokinin-like immunoreactivity in the cerebrospinal fluid was the same in freely-fed lactating and non-lactating rats. As in plasma, food deprivation markedly decreased the levels of cholecystokinin-like immunoreactivity in the cerebrospinal fluid of lactating rats but unlike in plasma, the levels were restored by feeding. The levels of cholecystokinin-like immunoreactivity were not changed under these conditions in the non-lactating rats. These results show that there is no correlation between the concentration of Cholecystokinin in plasma and cerebrospinal fluid, which supports the suggestion that the cholecystokinin-like immunoreactivity in the cerebrospinal fluid is derived from the brain. Removal of the litter from lactating rats deprived of food for 24 h reduced food intake and increased the concentration of cholecystokinin-like immunoreactivity in the cerebrospinal fluid, but not in plasma. The inhibition of food intake caused by an intraperitoneal injection of Cholecystokinin octapeptide increased after litter removal. It is suggested that hunger in the lactating rat is reflected by a decrease in the levels of cholecystokinin-like immunoreactivity in the cerebrospinal fluid and satiety by the restoration of these levels.  相似文献   

2.
The role of Cholecystokinin in a model of hypophagia, oestradiol-treated Ovariectomized rats, was investigated. Implantation of oestradiol-filled constant-release implants in rats made obese by ovariectomy potentiated the inhibitory effect of intraperitoneal injection of Cholecystokinin octapeptide on food intake after 24 h of food deprivation. The alterations in the concentration of Cholecystokinin in pjasma and of cholecystokinin-like immunoreactivity in cerebrospinal fluid produced by deprivation of food for 24 h and subsequent food intake for 1 h were unaffected by the oestradiol treatment as was the amount of food consumed during 1 h. Oestradiol-treated rats deprived of food for 6 h, however, consumed less food during a 15-min test than controls. Treatment with oestradiol blunted the decrease in the concentration of cholecystokinin-like immunoreactivity in the cerebrospinal fluid in response to 6 h of food deprivation. No alterations in the concentration of Cholecystokinin in plasma occurred after this period of food deprivation and subsequent feeding during 15 min in either oestradiol-treated or control rats. Thus, treatment with oestradiol enhances responsivity to exogenous Cholecystokinin octapeptide and changes the response of endogenous levels of cholecystokinin-like immunoreactivity in the cerebrospinal fluid to a short period of food deprivation. It is suggested that these effects are caused by an action of oestradiol on Cholecystokinin pathways in the brain. The results support the suggestion that hunger in the rat is inversely related to the decrease in the concentration of cholecystokinin-like immunoreactivity in the cerebrospinal fluid.  相似文献   

3.
Deprivation of food reduced the level of dopamine in the cerebrospinal fluid of male rats and subsequent ingestion of food or intraperitoneal injection of Cholecystokinin octapeptide restored the level. Injection of a dopamine receptor agonist (apomorphine) or Cholecystokinin octapeptide inhibited food intake and these effects were reversed by pretreatment with a dopamine receptor antagonist (cis-flupentixol). Blockade of cholecystokinin-A receptors, by treatment with L-364,718, but not cholecystokinin-B receptors, by treatment with L-365,260, blocked the inhibitory effect of Cholecystokinin octapeptide on food intake but did not affect the inhibitory effect of apomorphine. It is suggested that Cholecystokinin interacts with dopamine in the control of food intake.  相似文献   

4.
The involvement of dopamine receptors in the inhibitory effect of Cholecystokinin octapeptide on ingestive behaviour was investigated. Male rats were infused intraorally with a 1 M solution of sucrose and the amount ingested after treatment with the dopamine receptor agonist apomorphine was compared with that after treatment with Cholecystokinin octapeptide. The test allows a distinction between the consummatory aspects of ingestive behaviour, i.e. responses used to ingest food, from the appetitive aspects, i.e. responses used to obtain food, because it ignores the latter aspects. Comparisons were also made between the effects of apomorphine and Cholecystokinin octapeptide on pellet intake, a test in which the rat has to display appetitive ingestive behaviour. Injection of apomorphine (400 μg) increased the concentration of plasma apomorphine within 0.3 min and the concentration of dopamine in the cerebrospinal fluid within 1 min of injection and induced behavioural stereotypes within 10 min in food-deprived male rats. Plasma apomorphine and cerebrospinal fluid dopamine levels had decreased by 30 min and the behavioural stereotypies had decreased by 40 min after the injection. Injection of apomorphine also inhibited the consumption of food pellets and the ingestion of sucrose. Inhibition of pellet and sucrose ingestion paralleled the effect of apomorphine on Stereotypie behaviour. Thus, injection of a dopamine receptor agonist is followed by alterations in plasma levels of the agonist, cerebrospinal fluid dopamine levels and in Stereotypie and ingestive behaviour which occur in parallel, in an inverted U-shaped manner and with a temporal delay between each event. These results show a close correlation between dopamine receptor stimulation and inhibition of ingestive behaviour. However, reversal of the inhibitory effect of apomorphine on ingestive behaviour required pretreatment with a lower dose of a dopamine receptor antagonist (cis-flupentixol) (0.1 mg) than reversal of Stereotypie behaviour (0.8 mg). The effect of dopamine receptor stimulation on consummatory ingestive behaviour is thus relatively weak and not secondary to the induction of Stereotypic behaviour. Treatment with a high dose of cis-flupentixol (0.8 mg) caused a prolonged period of immobility but had no effect on the ingestion of sucrose. Dopamine receptor blockade, therefore, interferes with appetitive, but not consummatory ingestive behaviour. Injection of Cholecystokinin octapeptide (5 μg) suppressed pellet and sucrose intake in a manner comparable to that of apomorphine, but induced no behavioural stereotypes and caused a gradual, rather than inverted U-shaped, increase in the concentration of dopamine in the cerebrospinal fluid that did not correlate with the effect on ingestive behaviour. Furthermore, while the inhibitory effect of apomorphine on the ingestion of sucrose was reversed by pretreatment with a low dose of cis-flupentixol (0.1 mg), the inhibitory effect of Cholecystokinin octapeptide was only partially reversed by cis-flupentixol and a higher dose (0.8 mg) was required. Blockade of cholecystokinin-A receptors, by treatment with L-364,718, but not cholecystokinin-B receptors, by treatment with L-365,260, blocked the inhibitory effect of Cholecystokinin octapeptide and, by itself, L-364,718 increased the amount of ingested sucrose. The inhibitory effect of Cholecystokinin octapeptide on consummatory ingestive behaviour, which is mediated by cholecystokinin-A receptors, is likely to involve mechanisms in addition to dopaminergic ones.  相似文献   

5.
Recent studies have demonstrated the presence of fibres immunoreactive for somatostatin-28 (SS-28), which originate in the brainstem and selectively innervate the magnocellular oxytocin (OT) cells of the supraoptic nucleus. The potential physiological relevance of this pathway was investigated in the present study by measuring plasma OT levels in response to intraperitoneal administration of cholecystokinin in conscious male rats pretreated with intracerebroventricular injections of either SS-28 or artificial cerebrospinal fluid. Cholecystokinin treatment produced the expected marked rise in plasma OT levels in control rats pretreated intracerebroventricularly with artificial cerebrospinal fluid. However, this response was markedly blunted by prior intracerebroventricular administration of SS-28, even though SS-28 itself had no effect on basal plasma OT levels, nor did it impair OT release in response to hypertonic saline injection. These results demonstrate that centrally injected SS-28 can selectively block cholecystokinin-stimulated release of OT in rats, and support an inhibitory role for this peptide in brainstem-mediated neurohypophysial hormone secretion. Central SS-28 administration also elicited up to 3-fold increases in the amount of food ingested in 1 h by previously sated rats. These observations suggest the possibility that endogenous SS-28 may be involved in stimulating food intake in rats, and establish the basis for future studies to clarify the role of this neuropeptide in controlling ingestive behaviours.  相似文献   

6.
We compared changes in runway performance by rats for sucrose reward following injections of the synthetic C-terminal octapeptide of cholecystokinin (CCK-8) with those seen after variations in food deprivation and injections of lithium chloride. No effects on running for either 10% or 30% sucrose were found following 0.5 to 4.0 μg/kg of CCK-8, though such doses suppressed 30-min sucrose intake up to 53%. Statistically reliable slowing of running for 10% sucrose was observed on two series of tests after 8.0 μg/kg of CCK-8. Running for 30% sucrose was not significantly affected by this dose. The general ineffectiveness of CCK-8 for producing decrements in running spread contrasts with significantly reduced performance after either reductions in food deprivation (21 h vs 12 and 3 h) or injections of 75 mg/kg lithium chloride. These results suggest that the mode of action of CCK-8 in reducing food intake is different than that produced by changes in hunger or by non-specific interference with motivation by malaise. The finding that CCK-8 can substantially reduce consumption with no apparent changes in appetitive motivation is consistent with the hypothesis that this substance acts only late in the meal to prematurely trigger satiety.  相似文献   

7.
To study the possibility that release of dopamine in the brain mediates the inhibitory effect of Cholecystokinin octapeptide on ingestive behaviour, the effect of amphetamine on intake of pellets or an intraorally administered sucrose solution was compared with that of Cholecystokinin octapeptide. Additionally, comparisons were made between the effect of Cholecystokinin octapeptide and pargyline, a monoamine oxidase inhibitor, and α-methyl-ρ-tyrosine, a tyrosine hydroxylase inhibitor. While amphetamine dose-dependently inhibited pellet intake it failed to inhibit sucrose intake in doses which caused behavioural stereotypies (<800 μg). Cholecystokinin octapeptide (5 μg) inhibited ingestive behaviour in both tests. A very high dose of amphetamine (2 mg) was required to inhibit sucrose intake to a level comparable to that of Cholecystokinin octapeptide. Pargyline (5 to 25 mg) or α-methyl-p-tyrosine (25 to 100 mg) dose-dependently inhibited pellet intake but had only weak effects on the intake of sucrose. Pargyline increased the concentration of dopamine and 3-methoxytyramine in the dorsal striatum and decreased the concentration of 3,4-dihydroxyphenylacetic acid. α-Methyl-ρ-tyrosine decreased the concentration of dopamine and 3,4-dihydroxyphenylacetic acid, but not that of 3-methoxytyramine. Injection of amphetamine (2 mg), but not Cholecystokinin octapeptide, in rats pretreated with pargyline increased the concentration of 3-methoxytyramine in the dorsal striatum and this effect was blocked by pretreatment with α-methyl-ρ-tyrosine. Pretreatment with α-methyl-ρ-tyrosine partially reversed the inhibitory effect of Cholecystokinin octapeptide on sucrose ingestion, enhanced the effect of amphetamine but did not affect that of apomorphine, a dopamine agonist. The results support the possibility that the inhibitory effect of Cholecystokinin octapeptide on consummatory ingestive behaviour, in part, is mediated via release of dopamine in the brain.  相似文献   

8.
Male rats treated with reserpine were motionless and ingested only a few of ten consecutive intraoral injections of a 1 M solution of sucrose. While injection of apomorphine, a dopamine agonist, stimulated locomotion and stereotyped sniffing in reserpinized rats, it did not reactivate ingestive responses. The non-competitive N-methyl-D-aspartate receptor antagonist MK801, however, stimulated locomotion as well as ingestion suggesting involvement of glutamate in the suppressive effect of resperpine on ingestive responses. A series of experiments was therefore undertaken to investigate the possible physiological role of glutamate in feeding. For this purpose, we used Grill's intraoral intake test, in which the rat is infused intraorally with a sucrose solution and the amount ingested measured. In untreated rats, MK801 dose-dependently facilitated ingestion of the sucrose solution and antagonized inhibition of ingestion by cholecystokinin octapeptide. Administration of cholecystokinin octapeptide or ingestion of sucrose increased the concentration of glutamate in the nucleus of the solitary tract, a brain stem relay transmitting sensory information from the gastrointestinal tract to the forebrain. MK801 was found to bind specifically to this brain area and block the elevation of glutamate and dopamine levels which occurred after treatment with cholecystokinin octapeptide in this neural site. Together these data suggest that dopamine and glutamate may interact within the nucleus of the solitary tract in controlling ingestive behaviour.  相似文献   

9.
Cholecystokinin octapeptide and its analogue, caerulein, facilitated the K+-evoked release of 14C-GABA from tissue slices of rat parietal cortex. The effect of caerulein was maximal at 1 nM where an enhancement of 36% was produced. Cholecystokinin octapeptide gave rise to a similar maximal enhancement (29%), but was two orders of magnitude less potent. The enhancement of 14C-GABA release by caerulein was reversed by proglumide, a putative competitive antagonist at the cholecystokinin receptor. The possibility that the cholecystokinin-induced facilitation of GABA release in the cortex is involved in the anticonvulsant properties of cholecystokinin-like peptides is discussed.  相似文献   

10.
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