Pituitary lactotroph hyperplasia and chronic hyperprolactinemia in dopamine D2 receptor-deficient mice

被引:341
作者
Kelly, MA
Rubinstein, M
Asa, SL
Zhang, G
Saez, C
Bunzow, JR
Allen, RG
Hnasko, R
BenJonathan, N
Grandy, DK
Low, MJ
机构
[1] MT SINAI HOSP,DEPT PATHOL,TORONTO,ON M5G 1X5,CANADA
[2] OREGON HLTH SCI UNIV,CTR RES OCCUPAT & ENVIRONM TOXICOL,PORTLAND,OR 97201
[3] UNIV CINCINNATI,SCH MED,DEPT CELL BIOL,CINCINNATI,OH 45267
[4] UNIV CINCINNATI,SCH MED,DEPT ANAT,CINCINNATI,OH 45267
关键词
D O I
10.1016/S0896-6273(00)80351-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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 robe lactotroph hyperplasia without evidence of adenomatous transformation. Unexpectedly, the mutant mice had no hyperplasia of the intermediate robe 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.
引用
收藏
页码:103 / 113
页数:11
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