Deficiency of Dopamine in the Median Eminence of Snell Dwarf Mice*

Morgan, W. W.; Bartke, Andrzej; Pfeil, Karla A.

doi:10.1210/endo-109-6-2069

Cited by 44 publications

(34 citation statements)

References 16 publications

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“…Both types of effect are demonstrated in mice with spontaneous and lifelong PRL deficiency such as Snell [10, 24, 25]or Ames dwarfs [11, 26]. In these animals, hypothalamic TIDA neurons are not only deficient in DA levels [3, 4], but reduced in number [5, 6]. In adult Ames dwarf mice, PRL replacement increases DA and TH in extant neurons, but the number of detectable neurons is unaffected [9].…”

Section: Discussionmentioning

confidence: 99%

“…Although dwarf mice treated with ovine PRL or with grafts of normal anterior pituitary show increased body weights [3, 8, 37], the PRL effect on somatic growth may occur only when GH is also deficient, as in dwarfs.…”

Section: Discussionmentioning

confidence: 99%

“…Experimental PRL deficiency during early postnatal development, produced by treating lactating rats with bromocriptine, has been shown to result in decreased hypothalamic DA turnover and hyperprolactinemia in offspring [1, 2]. Dwarf mice that are deficient in PRL, GH and TSH exhibit, compared with normal siblings, not only severely reduced DA in the median eminence (ME) [3]and hypothalamus [4], but markedly lower numbers of TIDA neurons [5, 6]. The reduction in TIDA neuron number in dwarf mice has been shown to develop postnatally, coincident temporally with failure to initiate PRL production [4, 7].…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Prolactin Gene Disruption Does Not Compromise Differentiation of Tuberoinfundibular Dopaminergic Neurons

Phelps

Horseman²

2000

Neuroendocrinology

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“…Although a hypothalamic defect controlling growth-hormone production seems ruled out by the experiment of Garsner & Rennels (1960), a deficiency in hypothalamic dopamine may explain the prolactin deficiency (Morgan, Bartke & Pfeil, 1981). Bartke (1979) lists at least eleven fields of scientific investigation in which dwarfmice have been used as experimental animals.…”

Section: The Snell Dwarf Mousementioning

confidence: 99%

Mouse Mutants as Models in Endocrine Research

Charlton

1984

Exp Physiol

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Although Shire (1979) has listed some forty‐eight mouse mutants of interest to the endocrinologist, this short review has concentrated upon eleven mutations which have resulted in a significant number of scientific publications over the last 4 or 5 years. The selection of references has had to be limited, but it should be possible easily to expand the list given in this review. Although the proximate cause of none of the eleven mutations has been identified with certainty, the abnormalities of function have included hormone deficiencies and receptor and post‐receptor malfunctions. It is perhaps a reflexion on our society in the 1980s, that the bulk of research has concentrated on the obese mouse. However, we still do not know the initial cause of this syndrome. The major disadvantage of the mouse to the hormone assayist lies in the small blood volume and the extreme difficulty in taking serial blood samples over a short period of time. With increased sophistication of assay techniques this may prove less daunting, but is an area where a review of the literature reveals discrepancies between laboratories, and even between data generated by the same laboratory at different times. With regard to the hormone content of endocrine tissues, the way forward for peptide‐secreting glands may be in the measurement of mRNA levels for particular hormones. Certainly the methods of recombinant‐DNA technology will yield positive information upon the aetiology and expression of some of the syndromes considered above. Organ transplantation is an area in which mutant mice have proved useful, for example gonadal, pituitary and pancreatic tissue transplantation. The grafting of neural tissue in the hpg mouse has added a further dimension to this field of research. The great infrastructure of genetical research in mice has enabled us to breed mutant genes onto different genetic backgrounds. This area of research is one which deserves to expand. The techniues of in vitro fertilization, chimera formation and embryo transfer have been used, in part, in studies on mouse mutants, and should provide technical means for further investigating gene expression. The family of dwarf mutants are ideally suited for research into the expression of genes micro‐injected into the fertilized egg (see Charlton & Cox, 1983). As new hormones are isolated and become available for study these mouse mutants may well be useful in delineating physiological functions for natural and pharmacological products. Again, the dwarf mutants would seem ideally suited for research into the synthesis and action of GRF. Mouse mutants have proved of use to biochemists and embryologists and provide fertile ground for endocrine investigations ranging from molecular genetics to membrane biophysics.

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“…The purpose of this study was to examine the developmental pattern leading to low DA levels (18) and small TIDA population (16). Snell dwarf (Pit-1 dwj , dw/dw) and normal (DW/?)…”

Section: P Rolactin (Prl) Secretion By the Anterior Pituitarymentioning

confidence: 99%

Postnatal Regression of Hypothalamic Dopaminergic Neurons in Prolactin-Deficient Snell Dwarf Mice

Phelps

2004

Endocrinology

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Deficiency of Dopamine in the Median Eminence of Snell Dwarf Mice*

Cited by 44 publications

References 16 publications

Prolactin Gene Disruption Does Not Compromise Differentiation of Tuberoinfundibular Dopaminergic Neurons

Prolactin Gene Disruption Does Not Compromise Differentiation of Tuberoinfundibular Dopaminergic Neurons

Mouse Mutants as Models in Endocrine Research

Postnatal Regression of Hypothalamic Dopaminergic Neurons in Prolactin-Deficient Snell Dwarf Mice

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