Pituitary Lactotroph Hyperplasia and Chronic Hyperprolactinemia in Dopamine D2 Receptor-Deficient Mice
| Autor: | Malcolm J. Low, Carmen Sáez, Ge Zhang, Nira Ben-Jonathan, Marcelo Rubinstein, James R. Bunzow, Sylvia L. Asa, Richard G. Allen, David K. Grandy, Michele A. Kelly, Robert Hnasko |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Male
medicine.medical_specialty Neuroscience(all) Biology Prolactin cell 03 medical and health sciences Mice 0302 clinical medicine Sex Factors Dopamine Internal medicine Dopamine receptor D2 medicine Animals Autocrine signalling 030304 developmental biology 0303 health sciences Hyperplasia Receptors Dopamine D2 General Neuroscience medicine.disease Prolactin Mice Mutant Strains Hyperprolactinemia Melanotrophs Endocrinology Dopamine receptor Pituitary Gland Female 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Neuron. 19(1):103-113 |
| ISSN: | 0896-6273 |
| DOI: | 10.1016/s0896-6273(00)80351-7 |
| Popis: | Dopamine secreted from hypophysial hypothalamic neurons is a principal inhibitory regulator of pituitary hormone secretion. Mice with a disrupted D2 dopamine receptor gene had chronic hyperprolactinemia and developed anterior lobe lactotroph hyperplasia without evidence of adenomatous transformation. Unexpectedly, the mutant mice had no hyperplasia of the intermediate lobe melanotrophs. Aged female D2 receptor −/− mice developed uterine adenomyosis in response to prolonged prolactin exposure. These data reveal a critical role of hypothalamic dopamine in controlling pituitary growth and support a multistep mechanism for the induction and perpetuation of lactotroph hyperplasia, involving the lack of dopamine signaling, a low androgen/estrogen ratio, and a final autocrine or paracrine “feed-forward” stimulation of mitogenesis, probably by prolactin itself. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|