Deficits in motor coordination with aberrant cerebellar development in mice lacking testicular orphan nuclear receptor 4.

ABSTRACT: Since testicular orphan nuclear receptor 4 (TR4) was cloned, its physiological function has remained largely unknown. Throughout postnatal development, TR4-knockout (TR4-/-) mice exhibited behavioral deficits in motor coordination, suggesting impaired cerebellar function. Histological examination of the postnatal TR4-/- cerebellum revealed gross abnormalities in foliation; specifically, lobule VII in the anterior vermis was missing. Further analyses demonstrated that the laminations of the TR4-/- cerebellar cortex were changed, including reductions in the thickness of the molecular layer and the internal granule layer, as well as delayed disappearance of the external granule cell layer (EGL). These lamination irregularities may result from interference with granule cell proliferation withi

SUBMITTER: Chen YT 

PROVIDER: S-EPMC1061629 | biostudies-literature | 2005 Apr

REPOSITORIES: biostudies-literature