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M Leshem

Publications and source records attributed to M Leshem.

31 records · Page 2Linked to original sources
PubMed1993

Salt appetite consequent on sodium depletion in the suckling rat pup.

The ontogeny of the behavioral ability to compensate for sodium deficit was studied in the rat. The experiments showed that: 1) Before weaning age, sodium-depleted pups will increase their avidity for 3% NaCl solution; 2) the ability to select and drink a salt solution in response to a sodium deficit continues to evolve between 17-24 days of age, and that pups at these ages will modify their intake of salt and water as do adult rats when rectifying plasma osmolality; 3) The increased appetite for sodium is evident even when depleted preweanlings are dehydrated and provided with solid NaCl tablets to lick, showing that sodium appetite and hydrational status are already dissociated at this age; and finally, 4) sodium depletion first induces an increase in intake of orally infused 3% NaCl solution in 12-day-old pups. The picture of the development of salt appetite in the suckling rat that these findings present is of a precocious competence to meet a challenge to sodium homeostasis. In this respect salt appetite emerges in parallel to the other ingestive behaviors.

Animals↗
PubMed1990

Brain glucoprivation and ketoprivation do not promote ingestion in the suckling rat pup.

We examined the possibility that brain glucose or ketone availability may control suckling or precocious feeding in the preweanling rat. Brain glucoprivation induced by 5-thio-D-glucose injection into the 4th ventricle did not increase feeding on orally infused milk until 30 days of age, although hyperglycemia was evoked as early as 9 days by the same treatment. Plasma ketone levels varied with suckling status, but pharmacological blockade of hepatic free fatty acid oxidation, which restricts ketone availability (ketoprivation), failed to increase suckling. Because the suckling rat can switch energy substrates under nutritional duress, we combined glucoprivation and ketoprivation. Feeding was suppressed, and suckling was not affected. Finally, we injected ketones into the 3rd brain ventricle and found that they increased feeding. Thus, in contrast to the adult rat, reduced glucose or ketone utilization by the brain does not increase food intake in the preweanling, but increased circulating and brain ketone concentrations may arouse feeding.

Animals↗
PubMed1989

Ontogeny of renin-induced salt appetite in the rat pup.

Intracerebroventricular injections of renin in suckling rat pups increased intake of NaCl solutions when they were orally infused 5 hr after injection. The appetite for saline solution was evident in pups as young as 3 days, was greater in females, and was specific insofar as intake of milk, either by suckling or by oral infusion, was not affected. Three-day-old pups increased intake only to 12% NaCl, the acceptable concentration of NaCl becoming lower in older pups. These results suggest, first, that, as is true for feeding and drinking, the brain mechanism for salt appetite is competent for expression of the behavior in the very young rat pup, and second, that its angiotensinergic neural substrate is distinct from that which mediates the dipsogenic effect of the hormone.

Animals↗
PubMed1989

Cranial puncture, a simple procedure requiring no preparatory surgery: validation by observation of drinking and salt appetite evoked by intracerebroventricular renin.

A non-surgical procedure, "cranical puncture" (CP), for pulse intracerebroventricular (p.i.c.v.) injection of solutions in adult rats is described. The injections are made by pushing a needle through the scalp and skull while the rats are under brief carbon dioxide narcosis from which behavioral recovery is rapid. The method was validated by comparing the effects of renin injected either by CP or through conventional chronic ventricular cannulas. Renin injections by either procedure evoked copious drinking of water (224 +/- 23 ml/24 h) and 3% NaCl (44 +/- 9.1 ml/24 h) at smaller doses than previously reported. Cranial puncture is proposed as a simple method of i.c.v. injection for behavioral experimentation in rats, and its advantages are discussed.

Animals↗
PubMed1988

The ontogeny of drinking evoked by activation of brain angiotensin in the rat pup.

Renin (1 ng) was injected into the 3rd ventricle of the brain of rat pups at various ages, and their ingestion was measured by weighing them either after 40 min of oral infusion of water or milk while they were away from their dam (off-dam), or after 40 min of suckling from their dams (on-dam). Beginning at 3-5 days of age, renin increased ingestion of milk and water off-dam. After 15 days of age, milk ingestion off-dam was no longer increased by renin, but intake of water continued to be evoked. In contrast, renin did not increase intake by suckling at any age. These findings reveal that the adult characteristics of the dipsogenic action of the renin-angiotensin system in the brain emerge at 15 days, at which age the increased intake becomes entirely specific for water. This finding confirms the precocity of the neural controls of drinking in the rat and shows that, like the controls of independent feeding, they are dissociated from those of suckling. It adds support to the idea that the neonatal mammalian brain contains separate neurological systems for suckling and for independent ingestion.

Age Factors↗
PubMed1988

Thirst-induced anorexias and the ontogeny of thirst in the rat.

In previous work (Leshem, M., Boggan, B., and Epstein, A.N. (1988). The ontogeny of drinking evoked by activation of brain angiotensin in the rat pup. Dev. Psychobiol. Vol.21, pp. 63-75) we showed that thirst elicited by activation of the brain's renin-angiotensin system in the suckling becomes specific to water after 16 days of age. However, in the suckling, we did not find the anorexia that reportedly accompanies angiotensin-induced thirst in the adult. This suggests the existence of a further stage in the ontogeny of thirst. Therefore, the present study pursued the ontogeny of thirst and its effects on milk intake through prepubescence into adulthood. Experiment 1 revealed that intracranial renin does not cause an anorexia to milk in prepubescent or adult rats. Experiment 2 showed that the absence of anorexia is true of thirst induced by renin but not by cellular dehydration, although both dipsogens suppressed milk intake when rats also had water available. Experiment 3 confirmed that the preweanling shows anorexia to solid food, as does the adult. Together with other work, these findings suggest that the ontogeny of the thirsts aroused by renin or intracellular dehydration is complete before weaning.

Aging↗
PubMed1988

Morphine induces delayed anorexia in rats.

The delayed suppression of feeding caused by morphine was investigated in the rat. A single injection of morphine evoked a triphasic influence on feeding: a brief (1 h) severe anorexia was followed by hyperphagia (3 h) and a mild (20%) yet persistent (4-24 h) anorexia. This latter anorexic effect was at least partially naltrexone reversible, and the duration of this antagonism (8 h) was longer than that of naltrexone's anorexic effect (4 h). Delayed morphine anorexia cannot be ascribed to morphine's initial stuporific influence, and it was not dependent upon previous feeding or deprivation. It was not due to gastric distension. The specificity and significance of this anorexia is discussed.

Animals↗
PubMed1987

Brain serotonin depletion and nipple attachment in rat pups.

5,7-DHT (104 micrograms) was injected into the third brain ventricle of three-day-old rat pups 1 hr after desmethylimipramine pretreatment (20 mg/kg IP). Whole-brain serotonin was depleted by 50%, and there was some retardation of weight gain. Nipple attachment was observed in sucklings and in weaned pups. When 9 days old, attachment in 5-HT depleted pups was delayed and they were less active when undeprived, but not when 8 hr deprived. In comparison with pups raised in litters of 6 or 14, which served to control for reduced body weight, depleted pups' behavior was more similar to the heavier pups, suggesting that the behavioral differences were not due to retarded growth. After weaning at 21 days, depleted pups attached more up to 37 days of age, after which attachment was not reinstated by treatment with methysergide, suggesting that the waning of depletion induced attachment was not due to recovery of serotonergic function. Again, body weight controls showed that the effects were not due to retarded weight gain in the depleted pups. The results confirm the biphasic action of 5-HT antagonism on attachment, i.e., inhibition in the neonate and disinhibition in the weanling. The findings also show that central 5-HT systems are involved in the inhibition of attachment during weaning, but that this involvement is transient, and apparently not crucial.

5,7-Dihydroxytryptamine↗
PubMed1984

Suppression of feeding by naloxone in rat: a dose-response comparison of anorexia and conditioned taste aversion suggesting a specific anorexic effect.

The dose-related suppression of feeding by naloxone (0.25-15.0 mg/kg), either by injection before feeding, or by conditioning taste aversion (CTA), was compared. The weaker suppression found for CTA at low (below 0.75 mg/kg) and high (above 5.0 mg/kg) doses suggests that the aversive sequelae of naloxone injection cannot account fully for its suppressive effects. In turn, this suggests that naloxone exerts a specific anorexic effect. Comprehensive dose-response curves for naloxone anorexia (15 doses) and CTA (nine doses) are presented.

Analysis of Variance↗
PubMed1981

Morphine-induced anorexia in lateral hypothalamic rats.

The anorexic effect of morphine in rats with lateral hypothalamic lesions was examined. Morphine (15 mg/kg) produced an anorectic effect which was greater in lesioned rats than in controls. However, in lesioned rats, morphine anorexia was completely reversed by naloxone (2 mg/kg), while in controls there was mild anorexia. Repeated morphine injections caused decreasing anorectic effects, an effect which developed more rapidly in control than in lesioned subjects. The effects of morphine on food intake in lesioned rats were similar to the effects of fenfluramine, rather than amphetamine, suggesting involvement of serotonergic, rather than catecholaminergic mediation of morphine anorexia.

Amphetamine↗
PubMed1981

Ontogeny of fenfluramine and amphetamine anorexia compared in rat pups.

The anorexic effects of three doses of amphetamine or fenfluramine were compared in rat pups 5, 10, 15, 20 and 25 days of age. The anorexic effects of the drugs were monitored by weighing the pups before and after a 90 minute feeding period following four hours of deprivation. Amphetamine appeared to induce weight gain in 5-day-old rats, but at 10 days and thereafter, became progressively more potent in reducing weight gain and caused weight loss indicative of the involvement of non-specific factors. In contrast, while fenfluramine also reduced weight gain at 10 days, its potency was reduced in older pups and it did not cause weight loss. These results suggest that in rat pups amphetamine and fenfluramine act differently to reduce feeding and that brain serotonergic systems mediating inhibition of suckling are functional in 10-day-old rats. It is also argued that these findings lend credence to the notion that the ontogeny of feeding parallels its recovery after brain lesions.

Aging↗