Evidence of Prolactin Cell Deficiency in Connection With Low Reproductive Efficiency of Female `Torpid' Mice

Hc, Dung

doi:10.1530/jrf.0.0450091

Cited by 2 publications

(2 citation statements)

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“…Whether such a mechanism or an unbalanced hormonal situation could explain the failure to induce prolactin receptors in the liver of the male dwarf mouse remains unknown, as in normal males such receptors were readily detected. Dung (1975) has shown that prolactin cells constituted 10% of the entire cell population in the pituitary gland of dwarf mice, whereas in control mice the proportion was >40 %. The percentages of GH cells in the two groups were similar and this observation is consistent with the fact that the dwarf mouse is not totally deficient in GH (Sinha et al, 1975).…”

Section: Discussionmentioning

confidence: 99%

“…The mutant dwarf mouse inbred DW/J strain (mutant gene dwjdw) first reported by Snell (1929) is deficient in pituitary prolactin (Bartke, 1964(Bartke, ,1965aDung, 1975), whereas growth hormone (GH) is present in trace amounts in homogenates of pituitaries (Dung, 1975). A more recent report by Sinha, Salocks & Vanderlaan (1975), who used homologous radioimmunoassays, confirmed the lack of GH, particularly in males, as well as the profound deficiency of prolactin.…”

Section: Introductionmentioning

confidence: 99%

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Effect of prolactin and growth hormone on prolactin and LH receptors in the dwarf mouse

Bohnet¹,

Friesen²

1976

Reproduction

108

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Dwarf mice (DW/J; dw/dw) which exhibit a deficiency of prolactin and GH secretion were treated for 8 days with ovine prolactin and/or human GH (10 or 20 \g=m\g/day) and the effect on hepatic and testicular prolactin receptors was investigated. In both sexes there was a significant increase in body weight after all hormone treatments, but an increment in testicular weight was observed only after prolactin administration. Prolactin treatment increased the specific binding % of prolactin in liver membranes in females but not males, and in testicular homogenates (together with an increase in LH receptors). The results suggest that lack of prolactin but not of GH retards sexual development in these mice. Treatment with prolactin partly counteracts this deficiency, and the effect may be mediated by the induction of hepatic and testicular prolactin and LH receptors.

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Section: Discussionmentioning

confidence: 99%