Pituitary control of mouse testis in hereditary dwarfism: Histological and cytochemical observations

Cavallero, C; Martinazzi, M; Baroni, Carlo; Magrini, Umberto

doi:10.1016/0016-6480(63)90096-0

Cited by 12 publications

(11 citation statements)

References 18 publications

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“…If this was the case, sex drive was probably also augmented. Cavallero et al (1963) did not observe similar changes in spermatogenesis in dwarf mice after prolactin treatment. This was most likely due to the use of very young dwarfs, low doses of prolactin, a shorter period of treatment and gross histological rather than quantitative assessment of the response.…”

Section: Ratscontrasting

confidence: 47%

“…Cavallero, Martinazzi, Baroni & Magrini (1963) treated male dwarf mice with gonadotrophins and concluded that prolactin, like FSH, can increase testis weight and tubular size but cannot stimulate spermatogenesis or establish normal interstitial morph¬ ology. However, they noted that prolactin appeared to stimulate 'maturation of spermatocytes into spermatids'.…”

Section: Introductionmentioning

confidence: 99%

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Influence of Prolactin and Pituitary Isografts on Spermatogenesis in Dwarf Mice and Hypophysectomized Rats

Bartke¹,

Lloyd²

1970

Journal of Endocrinology

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This work was undertaken to study the influence of purified prolactin on spermatogenesis in hypophysectomized rats with or without testosterone propionate maintenance therapy and in prolactin-deficient hereditary dwarf mice. In addition some dwarf mice were given heterotopic isografts of non-dwarf mice pituitaries. In rats, 25 i.u. ovine prolactin given daily for 33 days had no effect on the maintenance of spermatogenesis. In untreated dwarf mice spermatogenesis progressed to completion but had a low yield due to cell loss, especially during premeiotic divisions. Both 10 i.u. prolactin daily for 28 days and pituitary grafts resulted in marked stimulation of spermatogenesis. The number of preleptotene and pachytene spermatocytes and step 7 spermatids was significantly increased in both inbred and F1 dwarf mice regardless of age. Since seminal vesicles were also considerably heavier in treated dwarfs, it was concluded that the observed stimulation of spermatogenesis was most likely due to elevated testicular androgen production indicating that, in the male mouse, prolactin may be involved in pituitary regulation of Leydig cell function.

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Section: Ratscontrasting

confidence: 47%

Section: Introductionmentioning

confidence: 99%

Influence of Prolactin and Pituitary Isografts on Spermatogenesis in Dwarf Mice and Hypophysectomized Rats

Bartke¹,

Lloyd²

1970

Journal of Endocrinology

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“…Several reports using various experimental models also show that PRL affects the population of spermatogenic cells. It is known that PRL stimulates the maturation of spermatocytes to spermatids in hereditary PRL-deficient mice but with no correlation to morphological changes in Leydig cells [38]. PRL also increases premeiotic spermatogonial division, meiotic prophase, meiosis and spermatid maturation at early stages in hypophysectomized rats [39].…”

Section: Discussionmentioning

confidence: 98%

Prolactin Induces Protamine 2 mRNA Expression in Rat Testis.

Hondo

Kobayashi

Ishiguro

et al. 1999

Journal of Reproduction and Development

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Abstract. The effect of prolactin on transcription during spermatogenesis was examined by subtractive DNA hybridization and differential screening. A protamine 2 cDNA fragment was isolated from one of the genes up-regulated in testes of rat 6 h after prolactin injection. In situ hybridization to detect protamine 2 mRNA was also performed using digoxigenin-labeled cRNA probes. Weak signals were detected from preleptotene to early pachytene spermatocytes, elongated spermatids and spermatozoa; strong ones were recognized from mid-to late-pachytene, diplotene, and secondary spermatocytes, and early round spermatids. Localization of protamine 2 mRNA coincided with that of prolactin receptor mRNA described in our previous report. We then compared the timedependent expression of protamine 2 mRNA with that of luteinizing hormone receptor mRNA after prolactin administration, using Northern blot analysis. Protamine 2 mRNA was up-regulated 1 h after the prolactin treatment, and stable levels were maintained for another 13 h. In contrast, luteinizing hormone receptor mRNA levels increased much later, at 13 h after prolactin injection. Therefore, protamine 2 gene responds rapidly to prolactin administration and up-regulation of expression appears to be independent of the luteinizing hormone pathway.

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“…It was thought that difficulty in obtaining food and water due to the behavioural abnormalities probably resulted in the growth retardation and death of the affected animals (Falconer, 1951;Searle, 1952;Snell, 1955;Chai, 1961) (Snell, 1929;Schaible & Gowen, 1961) (Smith & MacDowell, 1930, 1931Kemp, 1938;Osborn, 1938;Marshak, 1938;Francis, 1944Francis, , 1945Ortman, 1956;Rennels & McNutt, 1958;Elftman & Wegelius, 1959;Carsner & Rennels, 1960;Cavallero et al, 1963;Bartke, 1964Bartke, , 1965aBartke, , 1965bBartke, , 1965cBartke, , 1966aBartke, , 1966b. There is evidence to indicate that the high mortality of 'dwarf mice is related to a selective deficiency in the cellmediated type of immunity which is thymus-dependent (Baroni, 1967;Duquesnoy et al, 1970).…”

Section: Histological and Pathological Studiesmentioning

confidence: 99%

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

Hc¹

1975

Reproduction

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Pituitary control of mouse testis in hereditary dwarfism: Histological and cytochemical observations

Cited by 12 publications

References 18 publications

Influence of Prolactin and Pituitary Isografts on Spermatogenesis in Dwarf Mice and Hypophysectomized Rats

Influence of Prolactin and Pituitary Isografts on Spermatogenesis in Dwarf Mice and Hypophysectomized Rats

Prolactin Induces Protamine 2 mRNA Expression in Rat Testis.

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

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