Effects of Prolactin (PRL) on Pituitary and Testicular Function in Mice with Hereditary PRL Deficiency

Bartke, Andrzej; Goldman, Bruce D.; Bex, Frederick J.; Dalterio, S.

doi:10.1210/endo-101-6-1760

Cited by 94 publications

(51 citation statements)

References 25 publications

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“…The temporal difference observed in males and females for the samples taken at noon and midnight has also been found by Sinha, Salocks, Wickes & Vanderlaan (1977). In genetically prolactin-deficient mice, treatment with prolactin induces fertility and stimulates growth of the testes, testosterone production and spermatogenesis (Bartke, Goldman, Bex & Dalterio, 1977). Increased testosterone production at 30 days of age preceded a dramatic increase in prolactin at 35 days of age (Barkley, 1979) which coincided with rapid growth of the accessory organs in mice (Barkley & Goldman, 1977).…”

Section: Discussionmentioning

confidence: 59%

Peripheral plasma concentrations of LH, FSH, prolactin and GH from birth to puberty in male and female mice

Michael¹,

Kaplan²,

Macmillan³

1980

Reproduction

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Section: Discussionmentioning

confidence: 59%

Peripheral plasma concentrations of LH, FSH, prolactin and GH from birth to puberty in male and female mice

Michael¹,

Kaplan²,

Macmillan³

1980

Reproduction

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“…The previously published studies of PRL replacement in young dwarf mice indicated that PRL alone was sufficient to support TIDA neuron differentiation. Also, replacement of PRL alone has been shown to reinstate fertility in otherwise reproductively incompetent male dwarf mice [27]. Thus, in supporting either TIDA neuron development or reproductive competence, PRL replacement in PRL, GH and TSH deficiency has been shown to be sufficient, but PRL may not be specific in these roles.…”

Section: Discussionmentioning

confidence: 99%

Prolactin Gene Disruption Does Not Compromise Differentiation of Tuberoinfundibular Dopaminergic Neurons

Phelps

Horseman²

2000

Neuroendocrinology

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In mice with spontaneous mutations in transcription factors Prop-1 or Pit-1, the pituitary fails to produce prolactin (PRL), GH and TSH, and numbers of hypothalamic PRL-regulating dopaminergic (DA) neurons (area A12) are reduced by more than 50%. A normal neuronal population can be maintained in these mutants by PRL treatment of neonates, but not of adults. Targeted disruption of the PRL structural gene in mice provides a new model of isolated PRL deficiency to test the specificity of the PRL neurotrophic effect. The present study used morphological methods to assess hypophysiotropic tuberoinfundibular dopaminergic (TIDA) neurons in these mice, with the hypothesis that isolated PRL deficiency also would lead to reduction in TIDA neuron number. Brains of female and male homozygous PRL-null (–/–) mice and normal heterozygous (+/–) siblings were compared using formaldehyde-induced endogenous catecholamine fluorescence and tyrosine hydroxylase (TH) immunocytochemistry. Immunostaining intensity was quantified using computerized image analysis, and total numbers of TH-immunoreactive neurons were counted in three diencephalic DA brain regions. Intensity of DA fluorescence in A12 perikarya and median eminence (ME) was reduced in –/– mice; fluorescence in other brain areas was comparable for –/– and +/– mice. Immunostaining intensity of TH was significantly lower (p = 0.0001) in –/– than in normal mice in perikarya of A12, but not in cell bodies of nonhypophysiotropic area A13 (medial zona incerta). In external ME, TH immunostaining intensity was lower (p = 0.0001) in PRL-null than in normal mice. The decrease in TH intensity in both perikarya and in ME was significant for both female and male –/– mice. However, numbers of A12 neurons in the PRL-null mice were not lower than those of normal siblings. TH-immunoreactive cell number also did not differ between +/– and –/– mice in areas A13 and periventricular A14. The presence of a normal complement of A12 DA neurons in the PRL-null mice, despite greatly reduced DA and TH, emphasizes that steady-state content and differentiation of phenotype in individual neurons are very different assessments. The results suggest that, although absence of the stimulatory PRL feedback signal results in diminished activity of TIDA neurons, differentiation of these cells is not adversely affected.

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“…Both mutants have reduced circulating gonadotropins, yet Nr5a1 transcripts are elevated in the pituitary gland (8,73,84). The increase in Nr5a1 expression was expected because of absent antagonizing effects of Pit1 in the mutants (23).…”

Section: Experimental Design For Microarray Analysis Of Gene Expressionmentioning

confidence: 96%

“…These nonallelic mutants have many similar features. Both mutants have multiple pituitary hormone deficiency (MPHD) with little or no GH, PRL, or TSH, a reduction in circulating LH and FSH, and adult pituitary hypoplasia (8,16,84). Because of the similar hormone deficiencies, both mutants are the same size as their littermates at birth and begin to display obvious signs of growth insufficiency at ϳ2 wk of age.…”

mentioning

confidence: 99%

Candidate genes for panhypopituitarism identified by gene expression profiling

Mortensen¹,

MacDonald

Ghosh

et al. 2011

Physiological Genomics

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Mutations in the transcription factors PROP1 and PIT1 (POU1F1) lead to pituitary hormone deficiency and hypopituitarism in mice and humans. The dysmorphology of developing Prop1 mutant pituitaries readily distinguishes them from those of Pit1 mutants and normal mice. This and other features suggest that Prop1 controls the expression of genes besides Pit1 that are important for pituitary cell migration, survival, and differentiation. To identify genes involved in these processes we used microarray analysis of gene expression to compare pituitary RNA from newborn Prop1 and Pit1 mutants and wild-type littermates. Significant differences in gene expression were noted between each mutant and their normal littermates, as well as between Prop1 and Pit1 mutants. Otx2, a gene critical for normal eye and pituitary development in humans and mice, exhibited elevated expression specifically in Prop1 mutant pituitaries. We report the spatial and temporal regulation of Otx2 in normal mice and Prop1 mutants, and the results suggest Otx2 could influence pituitary development by affecting signaling from the ventral diencephalon and regulation of gene expression in Rathke's pouch. The discovery that Otx2 expression is affected by Prop1 deficiency provides support for our hypothesis that identifying molecular differences in mutants will contribute to understanding the molecular mechanisms that control pituitary organogenesis and lead to human pituitary disease.

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Effects of Prolactin (PRL) on Pituitary and Testicular Function in Mice with Hereditary PRL Deficiency

Cited by 94 publications

References 25 publications

Peripheral plasma concentrations of LH, FSH, prolactin and GH from birth to puberty in male and female mice

Peripheral plasma concentrations of LH, FSH, prolactin and GH from birth to puberty in male and female mice

Prolactin Gene Disruption Does Not Compromise Differentiation of Tuberoinfundibular Dopaminergic Neurons

Candidate genes for panhypopituitarism identified by gene expression profiling

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