These Drd2 knock-out mice exhibit chronic hyperprolactinemia and develop anterior lobe lactotrophhyperplasia. They may be useful for use in studies relating to effects of long-term therapy with D2 dopamine antagonists, and for testing new treatments for D2 agonist-resistant hyperprolactemia.
Dr. Malcolm J Low, University of Michigan Medical School
Mice with a disrupted D2 dopamine receptor gene display chronic hyperprolactinemia and develop anterior lobe lactotrophhyperplasia without evidence of adenomatous transformation. Homozygous mutant mice have no hyperplasia of the intermediate lobe melanotrophs. Aged female D2 receptor homozygous mice develop uterine adenomyosis in response to prolonged prolactin exposure. They also exhibit a locomotor deficit manifested as a 50% reduction in activity and decreased initiation of movement. Female homozygous mice develop prolactinomas of the anterior pituitary gland. Homozygous mice exhibit decreased sensitivity to the rewarding and locomotor effects of ethanol.
|Allele Name||targeted mutation 1, Malcolm J Low|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||D2-; D2 KO; D2KO; D2R-; Drd2-|
|Gene Symbol and Name||Drd2, dopamine receptor D2|
|Strain of Origin||129S2/SvPas|
|Molecular Note||A genomic fragment containing exon 7 and part of exon 8 was replaced by a neomycin resistance cassette.|
|Mutations Made By|| |
Dr. Malcolm Low, University of Michigan Medical School
When maintaining a live colony, these mice can be bred as homozygotes.
The Donating Investigator reports that homozygous females will have fewer repeat litters than the heterozygotes. The expected coat color from breeding is black.
When using the D2- mouse strain in a publication, please cite the originating article(s) and include JAX stock #003190 in your Materials and Methods section.