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Biomedical subjects

H Moltz

Publications and source records attributed to H Moltz.

At least 37 records · Page 2Linked to original sources
PubMed1984

Altered bile acid physiology during lactation in the rat.

There is evidence that the rate of bile acid secretion increases significantly during lactation in the rat. We show that this increase in secretion rate is accompanied by an expanded bile acid pool and that occasioning the enhancement of both pool size and secretion is an increase in bile acid synthesis. The hypothesis is advanced that maternal prolactin, promoted by suckling young, amplifies cholesterol-7-alpha-hydroxylase, the rate-limiting enzyme in bile acid biosynthesis, and perhaps HMG-CoA reductase, the rate-limiting enzyme in cholesterogenesis.

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PubMed1983

The maternal pheromone of the rat: testing some assumptions underlying a hypothesis.

Herein we report four experiments relating to the maternal pheromone of the rat that show (a) preweanling young consume pheromone-containing feces most conspicuously between 14 and 27 days; (b) they consume those feces preferentially; (c) such feces contain high levels of deoxycholic acid; and (d) preweanling young are deficient in deoxycholic acid. The data of these experiments lend support to the hypothesis that in responding to the pheromone the young ingest deoxycholic acid, a steroid believed to promote gut immunocompetence and brain myelination.

Animals↗
PubMed1982

Manipulation of testosterone in the neonatal rat and pheromonal emission in the adult.

The question we addressed is why the male rat fails to emit the maternal pheromone when caring for young or when injected with prolactin. Our hypothesis was that exposure to androgen neonatally decreases the prolactin sensitivity of the male liver, making that liver incapable of secreting sufficient cholic acid for pheromonal synthesis. Accordingly, we castrated male rats prior to 2 hr of age and injected female rats with testosterone propionate within 8 days of age. Only those animals that had been spared exposure to androgen neonatally showed evidence of the pheromone when injected with prolactin as adults. Moreover, these same animals exhibited a higher output of cholic acid per g liver than their control counterparts (sham-operated males and vehicle-injected females). We conclude that the sex-related capacity for pheromonal emission is differentiated perinatally and involves the sensitivity of the liver to prolactin and its consequent secretion of cholic acid.

Animals↗
PubMed1982

The maternal pheromone of the rat as an innate stimulus for pre-weanling young.

We undertook to determine whether previous exposure in the nest is necessary to establish the attractiveness of the maternal pheromone or whether that attractiveness is innately based. In Experiment I we showed that the pheromone is a prepotent stimulus insofar as it is approached in preference to a different but equally familiar odor. Experiment 2 demonstrated that when pups are denied previous exposure to the pheromone they nonetheless approach the pheromone preferentially in a choice test involving a pheromone-emitting and a non-pheromone-emitting female. And finally, in Experiment 3, we again used pups that had been isolated from the pheromone. Here, however, the choice was between a pheromone-emitting female and a female which, while non-pheromone-emitting, carried a thoroughly familiar nest odor. The pups decisively chose the pheromone-emitting female. We conclude that pheromonal attractiveness is innately based and suggest that the pheromone itself may have been selected as a signal during the course of evolution.

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PubMed1982

Reduced prolactin binding to liver membranes during pheromonal emission in the rat.

Between 14 and 27 days of lactation, female rats excrete a pheromone in their feces that is cholic-acid dependent and that strongly attracts young. Previous research has shown that high circulating levels of prolactin are necessary before the pheromone can be emitted. However, during the time of pheromonal emission prolactin in serum conspicuously declines, while in hepatic cytosol the hormone reaches peak levels. We were interested in the question of how the liver can show peak cytosolic concentrations of prolactin at a time of falling blood levels of prolactin. Accordingly, we examined the prolactin binding capacity of liver membrane fractions during selected periods of lactation. We also studied the livers of virgin and pregnant females for comparison. Three membrane fractions were separated: the cell membrane, the nuclear membrane and a fraction consisting of the cell membrane and large non-nuclear organelles. In all three fractions, there was an increase in available and total prolactin binding in the liver when pregnant females were compared with nulliparous females. However, during the time of pheromonal emission, when prolactin in hepatic cytosol was elevated, there was a significant reduction in the prolactin binding capacity of the liver. How such a reduction increases the cytosolic concentration of the hormone and in turn heightens cholic acid output and pheromonal emission remains unsolved.

Animals↗
PubMed1980

The maternal pheromone and bile acids in the lactating rat.

Bile was drawn from virgin rats and from postpartum rats that were with young for 5, 12, 21, and 30 days, respectively. The bile thus drawn was analyzed enzymatically after chromatographic separation to test an hypothesis relating cholic acid and one of its metabolites, deoxycholic acid, to the appearance of the maternal pheromone. Our finding that cholic acid, but not deoxycholic acid, reached a peak that was tied specifically to the period of pheromonal emission led us to advance a revised hypothesis. We now think that cholic acid alone, or more likely a cholic metabolite other than deoxycholic acid, underlies the appearance of the pheromone.

Animals↗
PubMed1979

Initiation of maternal behavior in the rat: possible involvement of limbic norepinephrine.

The dorsal norepinephrine (NE) fiber system was manipulated in pregnant female rats. Brainstem lesions of the dorsal bundle, depleting NE in cortex and hippocampus, resulted in deficits in maternal-behavior onset in primiparous rats. Similarly, fornix-bundle transections, depleting only hippocampal NE, were associated with an absence of pup care. Hypothalamic NE levels, as well as dopamine and serotonin concentrations in cortex, hippocampus and hypothalamus, were not significantly affected by these manipulations. The data are discussed in terms of behavioral specificity, possible hormonal involvement and interactions with diencephalic mechanisms controlling the onset of maternal behavior in the female rat.

Animals↗
PubMed1978

Serotonergic mediation of the suckling-induced release of prolactin in the lactating rat.

Lactating female rats were infused with the serotonergic neurotoxin, p-chloramphetamine (PCA), via stainless steel cannulae implanted into either the 3rd or the lateral ventricle. Those mothers receiving the drug in the 3rd ventricle sustained a more severe depletion of hypothalmic serotonin (43% vs 23%) and a significantly greater incidence of pup mortality (98% vs 48%) than those receiving the drug in the lateral ventricle. Coincident with the depletion of hypothalmic serotonin was a reduction in serum prolactin (Prl). Subcutaneous (s.c.) infections of Prl into each group of females sharply reduced the number of pup deaths. It was concluded that hypothalmic serotonergic neurons mediate the suckling-induced release of Prl necessary for the maintenance of lactation.

Animals↗
PubMed1978

Concentration and metabolism of serotonin in selected brain areas during pregnancy and lactation in the rat.

Serotonin (5-HT) and its major metabolite, 5-hydroxyindole acetic acid (5-HIAA), were assayed in hypothalamus, hippocampus, and cortex during selected stages of pregnancy and lactation in the rat. No changes in 5-HT were observed in any of the brain areas analyzed. However, concentrations of 5-HIAA in hypothalamus and hippocampus, though not in cortex, showed marked changes during the immediate postpartum period. The significance of these changes is discussed in terms of possible hormone-neurotransmitter relationships.

Animals↗
PubMed1977

Bile, prolactin, and the maternal pheromone.

When bile from females that had been lactating for 21 days was injected into the cecum of male rats it induced release of a maternal pheromone. Males injected with bile drawn from females in which prolactin had been inhibited, or from females that had been lactating for only 5 days, did not emit the pheromone. These data suggest a sex difference in the way prolactin alters the composition of bile so that the female can emit the maternal pheromone while the male normally cannot.

Animals↗
PubMed1977

Effects of central norepinephrine depletion on the initiation and maintenance of maternal behavior in the rat.

The catecholaminergic neurotoxin, 6-hydroxydopamine (6-OHDA), was used to test the hypothesis that increased transmission across selected noradrenergic synapses is involved in the initiation of maternal behavior. Specifically, 6-OHDA was infused intraventricularly either two days before parturition or four days after parturition. Control animals were infused with the vehicle alone. Among prepartum animals, NE depletion of more than 30% of control levels interfered with the initiation of maternal behavior. Among lactating animals, similar degrees of NE depletion had no significant effect on the maintenance of maternal behavior. Thus, NE appears to be involved in the initiation of maternal behavior, but not in the maintenance of the behavior once that behavior is established.

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