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Prolactin receptor signal transduction pathways and actions determined in prolactin receptor knockout mice
P A Kelly1, N Binart, M Freemark
1INSERM Unité 344-Endocrinologie Moléculaire, Faculté de Médecine Necker, 156 rue de Vaugirard, 75730 Paris Cedex, France. kelly@necker.fr
Abstract:
Prolactin-receptor-deficient mice are a good model in which to study the various actions of prolactin. Female homozygous knockout mice are completely infertile and show a lack of mammary development, while hemizogotes are unable to lactate following their first pregnancy. Male and female homozygotes have markedly elevated serum prolactin levels, and in some instances pituitary hyperplasia is present. Maternal behaviour is severely affected in both hemizygous and homozygous animals. Bone formation is reduced in young animals and in adults (males and females). Finally, older males and females show a slight reduction in body weight, which seems to be due to reduced abdominal fat deposition in the knockout animals.
Insights
Prolactin-receptor-deficient mice exhibit infertility, impaired mammary development, and altered maternal behavior. These mice also show reduced bone formation and body weight, highlighting prolactin
Area of Science:
- Endocrinology
- Reproductive Biology
- Animal Models
Background:
- Prolactin is a key hormone regulating reproduction, metabolism, and behavior.
- Understanding prolactin's functions requires appropriate animal models.
- Prolactin receptor signaling is crucial for mediating prolactin's effects.
Purpose of the Study:
- To investigate the physiological roles of prolactin using prolactin-receptor-deficient mice.
- To characterize the reproductive, developmental, and metabolic consequences of prolactin receptor deficiency.
Main Methods:
- Generation and characterization of homozygous and hemizygous prolactin-receptor knockout mice.
- Assessment of fertility, mammary gland development, lactation, and maternal behavior.
- Analysis of serum prolactin levels, pituitary morphology, bone formation, and body weight.
Main Results:
- Homozygous females were infertile with absent mammary development; hemizygotes failed to lactate.
- Elevated serum prolactin and occasional pituitary hyperplasia observed in homozygotes.
- Impaired maternal behavior, reduced bone formation, and decreased body weight (due to fat reduction) in knockout mice.
Conclusions:
- Prolactin receptor signaling is essential for female fertility, lactation, and maternal care.
- Prolactin plays a significant role in bone metabolism and body weight regulation.
- Prolactin-receptor-deficient mice serve as a valuable model for studying prolactin's diverse physiological actions.