Hypothalamic stimulation induces vagally mediated hypocalcemia in the rat

Ma, Jingyi; Aou, Shuji; Hori, Tetsuro

doi:10.1016/0361-9230(94)90049-3

Cited by 9 publications

(5 citation statements)

References 33 publications

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“…After ip injection, exogenous rPRL bind to PRLR(L) in the CP to exert the antistress effect by the same mechanism. Similarly, after icv injection, exogenous rPRL bind to PRLR(L) in the PVN to exert the antistress effect through vagus nerves (47,48).…”

Section: Acknowledgmentsmentioning

confidence: 99%

Prolactin Prevents Acute Stress-Induced Hypocalcemia and Ulcerogenesis by Acting in the Brain of Rat

et al. 2004

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Stress causes hypocalcemia and ulcerogenesis in rats. In rats under stressful conditions, a rapid and transient increase in circulating prolactin (PRL) is observed, and this enhanced PRL induces PRL receptors (PRLR) in the choroid plexus of rat brain. In this study we used restraint stress in water to elucidate the mechanism by which PRLR in the rat brain mediate the protective effect of PRL against stress-induced hypocalcemia and ulcerogenesis. We show that rat PRL acts through the long form of PRLR in the hypothalamus. This is followed by an increase in the long form of PRLR mRNA expression in the choroid plexus of the brain, which provides protection against restraint stress in water-induced hypocalcemia and gastric erosions. We also show that PRL induces the expression of PRLR protein and corticotropin-releasing factor mRNA in the paraventricular nucleus. These results suggest that the PRL levels increase in response to stress, and it moves from the circulation to the cerebrospinal fluid to act on the central nervous system and thereby plays an important role in helping to protect against acute stress-induced hypocalcemia and gastric erosions.

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Section: Acknowledgmentsmentioning

confidence: 99%

Prolactin Prevents Acute Stress-Induced Hypocalcemia and Ulcerogenesis by Acting in the Brain of Rat

et al. 2004

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“…However, the involvement of other organs in the regulation of blood calcium level is not clearly understood. It has been reported that some gastric factors reduce blood calcium levels and that vagally mediated hypocalcemia is induced by hypothalamic stimulation (1)(2)(3). Another etiologic organ is the pancreas.…”

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confidence: 99%

Molecular Cloning and Expression of Serum Calcium- decreasing Factor (Caldecrin)

Tomomura

Fukushige

et al. 1995

Journal of Biological Chemistry

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We previously reported on the purification of a serum calcium-decreasing factor, referred to as caldecrin, from porcine pancreas, that is thought to be a serine protease (Tomomura, A., Fukushige, T., Noda, T., Noikura, T., and Saheki, T. (1992) FEBS Lett. 301, 277-281). In the present study, we purified caldecrin from rat pancreas and determined its primary structure by cDNA cloning. The predicted caldecrin protein is presumed to be synthesized as a preproenzyme of 268 amino acids with a signal peptide of 16 amino acids and an activation peptide of 13 amino acids, and is, with the exception of a central region, almost identical to the reported rat pancreatic elastase IV sequence. The caldecrin gene is selectively expressed in the pancreas, as judged by Northern blot analysis. After expression in BMT-10 cells, immunoreactive caldecrin was found in the culture supernatant, and it inhibited the parathyroid hormone-stimulated 45 Ca release from cultured fetal long bones. Catalytic site mutants were synthesized in a baculovirus system, and recombinant mutants also decreased the serum calcium level of mice. These data implicate caldecrin, a protease closely related to elastase IV, in the regulation of blood calcium levels.

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“…Each rat was exposed to 1 trial of forced swimming, as previously described (Ma et al, 1994;Pare, 1989aPare, , 1989bFujimoto et al, 2006). The water tank, consisting of a cylindrical acrylic container (50 cm high, 30 cm in diameter), was filled 35 cm deep with tap water (24 ± 1°C).…”

Section: Forced Swimming Test (Fst)mentioning

confidence: 99%

Postnatal exposure to low-dose bisphenol A influences various emotional conditions

et al. 2013

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-Bisphenol A (BPA) is one of the 'environmental endocrine disrupters' (EEDs) released by plastics and resin known to interfere with hormonal responses. In this study, female Wistar rats were exposed to low-dose BPA (24 μg/kg/day) during 7 days after giving birth. The male and female offspring, exposed to the BPA through lactation, were evaluated using an open field test (OFT) at the age of six weeks, an elevated plus maze test (EPM) at seven weeks, and a forced swimming test (FST) at nine weeks. The OFT indicated that females were more active than males, and that BPA selectively increased rearing duration in males, thereby eliminating the gender effect. The results of EPM showed that BPA did not enhance the anxiety-like action; rather, it was associated with an anxiolytic-like action in females. In the FST, not only there was an increase in the immobility time, but also there was reduction of latency observed in BPA rats. It indicated that the depression-like responses were clearly enhanced by the postnatal exposure. Altogether, these data suggest that low-dose BPA ingested by neonates through breastfeeding may cause persistent aberrant behaviors that are relevant to emotions.

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Hypothalamic stimulation induces vagally mediated hypocalcemia in the rat

Cited by 9 publications

References 33 publications

Prolactin Prevents Acute Stress-Induced Hypocalcemia and Ulcerogenesis by Acting in the Brain of Rat

Prolactin Prevents Acute Stress-Induced Hypocalcemia and Ulcerogenesis by Acting in the Brain of Rat

Molecular Cloning and Expression of Serum Calcium- decreasing Factor (Caldecrin)

Postnatal exposure to low-dose bisphenol A influences various emotional conditions

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