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Biomedical subjects

I H Gispan

Publications and source records attributed to I H Gispan.

7 recordsLinked to original sources

Release of endogenous cholecystokinin in response to gastric preloads in rats on postnatal days 9--12.

Release of endogenous cholecystokinin (CCK) from the small intestine by gastric loads was investigated in rats on postnatal days 9--12 (P9--P12). After 5--6 h of deprivation, pups received 5% b.wt. loads of water, 0.9% NaCl, 20% glucose, 20% maltose, 200 mg soybean trypsin inhibitor (SBTI) in 0.9% saline or sham load. Plasma was collected 15 min after the loads, and the concentration of bioactive CCK was measured by a specific and sensitive bioassay. Loads of SBTI and water significantly increased plasma CCK compared to sham loads, but loads of saline, glucose, and maltose did not. The efficacy of the water load was not demonstrated in adult rats. The results suggest that the previously reported reduction of intake during independent ingestion by hypertonic preloads of glucose and maltose was not mediated by the release of CCK sufficient to be detected in the plasma under these conditions.

Animals↗

Examining the role of cholecystokinin in appetitive learning in the infant rat.

The role of Cholecystokinin (CCK), a gut hormone and neuropeptide, in early learning was examined. Pairing a novel odor (presented away from the nest) with exogenously administered CCK (0.25 & 0.5 microg/kg IP) has been shown to produce a conditioned-odor preference in infant rats (Weller, A.; Blass, E.M. Behav. Neurosci. 104:199-206; 1990). This suggests that CCK can act as a positive unconditioned stimulus (UCS). In the present study the possibility that CCK mediates learning was examined in 12-day-old rats, using rewards that represent aspects of the dam and the nest. In Experiments 1 and 2, pups received the selective CCK1 receptor antagonist devazepide (600 microg/kg), the selective CCK2 receptor antagonist L365,260 (600 microg/kg), or vehicle. In a series of training trials, choosing a particular floor texture was rewarded by 20 sec. on a rug texture (experiment 1) or with maternal (feces) odor (experiment 2). In experiment 3, after administering devazepide (0, 600, or 1000 microg/kg) a novel odor was paired once with reunion of the pup with its dam. The dependent measure in all studies was the pup's relative preference toward the (tactile or olfactory) conditioned stimulus (CS), determined in preference tests. Conditioned preferences were evident in all experiments. The CCK receptor antagonists did not increase conditioned preference levels. L365, 260 (experiment 2) and devazepide (experiment 1) clearly blocked the appearance of the conditioned effect in one of the experiments. In addition, devazepide treatment eliminated the conditioned effect in the two other experiments, by increasing preference levels in the control groups. In summary, the results suggest that endogenous CCK mediates some aspects of the infant's acquisition of new associations. The role of the two receptor-subtypes appears to be different, depending on the context and the nature of the rewarding stimulus.

Animals↗

Ontogeny of hypertonic preabsorptive inhibitory control of intake in neonatal rats.

The ontogenetic development of postingestive inhibitory control of ingestion by the osmotic load of a preload was examined in rats. On postnatal days 6 (P6) and 12 (P12), pups were deprived for either 6 or 24 h. Gastric preloads (5% body wt) of water, mannitol (a sugar alcohol that is not absorbed) in six concentrations [from 0.125 M (hypotonic) to 1.0 M (hypertonic)], or sham preloads were administered 5 min before a 30-min intake test. Compared with sham treatment, isotonic mannitol (0.25 M), a probe of volumetric control, significantly reduced intake on P12, but not on P6. Compared with isotonic mannitol, the three highest hypertonic concentrations (0.5, 0.66, and 1.0 M) significantly decreased intake on P12, at both levels of deprivation. On P6, 0.66 and 1.0 M mannitol reduced intake after 24 h, but not after 6 h, of deprivation. Thus, on P6, the hypertonic control was detectable only after prolonged deprivation and the volumetric control was not present. On P12, both controls were observed and the hypertonic control was more potent than on P6.

Absorption↗

A cholecystokinin receptor antagonist blocks milk-induced but not maternal-contact-induced decrease of ultrasonic vocalization in rat pups.

The role of cholecystokinin (CCK) in reducing separation-induced ultrasonic vocalization (USV) was examined by peripheral administration (of the selective CCK(A) receptor antagonist devazepide to 10-11-day-old rats. Pups placed alone for 2 min emitted a mean of 55.1 USV/min. When placed on a paper towel wet with warm, sweet milk, USV rate decreased to 23.2/min for the following 8 min. Devazepide (150-600 microg/kg IP) prevented this USV reduction, but did not increase feeding. In contrast, USV reduction produced by contact with the anesthetized dam was not affected by devazepide. Similarly, the opiate antagonist naltrexone (0.5 and 1.0 mg/kg) has been shown to block morphine-induced USV decrease in pups away from the dam, but was ineffective when USV reduction was induced by the presence of the dam (Blass et al., 1990; Carden & Hofer, 1990). The current findings suggest that CCK's role is specific, in that it mediates milk- but not dam-induced quieting of USV. The results, however, are not incompatible with the possibility that CCK and opioids are part of multiple, redundant pathways that mediate the quieting of USV by the dam.

Animals↗

Characteristics of glucose and maltose preloads that inhibit feeding in 12-day-old rats.

Nonvolumetric inhibitory control of food intake during independent ingestion was studied in rats on postnatal day 12. Pups received either sham intubation or equivolumetric (5% BW) preloads of 20% (w/v) glucose, 20% maltose, 20% 2-deoxy-D-glucose (2-DG), 0.9% NaCl, 200 mg soybean trypsin-inhibitor (SBTI) or distilled water, 5 min prior to 30-min access to a milk diet spread on the floor of a beaker. To investigate if endogenous cholecystokinin mediated any of the inhibitory effects of the preloads on intake, pups were injected IP with 1 mg/kg devazepide, a specific CCK(A) receptor antagonist, or with vehicle 30 min prior to the intake test. All preloads reduced intake (measured by percent body weight gain) compared to sham intubation. Glucose (20%) reduced intake significantly more than 0.9% saline, but not more than the preload of 20% 2-DG. This suggests that the effect of glucose can be accounted for by its preabsorptive osmotic properties because 2-DG is not actively transported or metabolized. The inhibitory effect of 20% maltose may also be due to its osmotic load, but these experiments did not provide clear evidence for this. Cholecystokinin apparently did not mediate the effect of any of the preloads except SBTI, because devazepide only reduced the inhibition produced by a preload of SBTI. These results provide further evidence that hypertonic stimuli in the stomach or small intestine provide inhibitory control of food intake by postnatal day 12.

Animals↗

Preloads of corn oil inhibit independent ingestion on postnatal day 15 in rats.

The ontogenetic development of postingestive inhibitory control of ingestion by an oil preload was examined in preweaning rats. Gastric preloads (5% b.wt) of water, mineral oil or corn oil were administered 5 min before a 30-min intake test in which pups licked milk from the floor of a test chamber. Preloads of corn oil decreased intake significantly compared with preloads of mineral oil or water on Postnatal Days 15 and 18, but not on Postnatal Day 12. Because preloads of corn oil reduced intake ore than preloads of mineral oil, it is possible that the inhibitory effect of corn oil is due to its fats rather than to its oily texture. Cholecystokinin (CCK), presumably released from the small intestine, apparently mediates part of this inhibitory effect because pretreatment with devazepide, a specific CKKA antagonist, significantly reduced the inhibition produced by corn oil.

Age Factors↗

Postingestive inhibitory controls of independent ingestion in 12-day-old rats.

The postingestive inhibitory control of independent ingestion produced by gastric preloads was investigated in 12-day-old Sprague-Dawley rats. Pups received isovolumetric (5% of body weight) preloads of saline (0.9%), glucose (5%, 10%, or 20%) or maltose (5%, 10%, or 20%) 5 min before a 30-min independent ingestion test in which pups licked milk from the floor of the test chamber. All preloads reduced intake significantly compared to the control condition in which pups were intubated, but no preload was administered. The reduction of intake produced by the isovolumetric, isotonic solutions (saline, 5% glucose, and 10% maltose) is consistent with the stimulation of a preabsorptive, inhibitory mechanism sensitive to volume. The significantly larger reduction of intake produced by isovolumetric, hypertonic solutions (20% glucose and 20% maltose) is consistent with the stimulation of an additional postingestive inhibitory mechanism sensitive to the osmotic, saccharidic, or, in the case of 20% glucose, metabolic properties of these solutions. Because preloads were given 5 min prior to the intake tests, it is likely that the site of action of both inhibitory mechanisms was preabsorptive, although a postabsorptive site for part of the inhibitory effect of 20% glucose cannot be excluded.

Animals↗