Hormonal and morphological study of the pituitaries in reeler mice.
Reelin is a neuronal glycoprotein that plays a crucial role in brain layer formation during prenatal development. The reeler mutant mouse lacks Reelin, leading to abnormalities in the neuronal layering of cerebral cortex and cerebellum, producing ataxia, tremor and abnormal locomotion. Reeler mice are reported to have growth retardation and most of them are sterile or unable to bring up their newborns. Since the brain is one of the main regulator of pituitary hormone secretion and no information was reported regarding pituitary function and structure in these mutant mice, we studied pituitary endocrine activity and morphology in reeler mice. Mice were classified in three groups as reeler homozygote (RHM), reeler heterozygote (RHT) or control (CO). Pituitary hormone blood levels were assessed by enzyme immunoassay (EIA) and immunoradiometric assay (IRMA). Animals and their pituitaries were weighted and pituitaries were studied by histology, immunohistochemistry and electron microscopy. Results showed statistically significant differences in body weight and in adrenocorticotropic hormone (ACTH) and luteinizing hormone (LH) blood levels between the three groups. In contrast, growth hormone (GH) blood levels showed a high individual variation and no decrease in reeler groups compared with CO. Morphological studies revealed no differences in pituitary cell types except that somatotrophs appeared to be slightly smaller in RHM and RHT. Although it seems that pituitary hypofunction is not responsible for growth retardation, more studies are needed to obtain a deeper insight into the endocrine status of these mutant mice to elucidate the cause of their low body weight and reproductive behaviour.
Lombardero
Matilde
M
Department of Anatomy and A.P., Faculty of Veterinary Sciences, University of Santiago de Compostela, Lugo, Spain. mlomba@lugo.usc.es
Kovacs
Kalman
K
Horvath
Eva
E
Salazar
Ignacio
I
D000324:Adrenocorticotropic Hormone / Q000032:analysis; D000818:Animals; D005640:Follicle Stimulating Hormone / Q000032:analysis; D006130:Growth Disorders / Q000378:metabolism / Q000473:pathology; D013006:Growth Hormone / Q000032:analysis; D006579:Heterozygote; D006720:Homozygote; D007150:Immunohistochemistry; D007986:Luteinizing Hormone / Q000032:analysis; D051379:Mice; D008818:Mice, Neurologic Mutants / Q000235:genetics / Q000378:metabolism*; D046529:Microscopy, Electron, Transmission; D010903:Pituitary Gland, Anterior / Q000378:metabolism* / Q000473:pathology*; D010907:Pituitary Hormones / Q000032:analysis*; D011388:Prolactin / Q000032:analysis; D000091042:Reelin Protein; D013972:Thyrotropin / Q000032:analysis
D010907:Pituitary Hormones; D000091042:Reelin Protein; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D013006:Growth Hormone; C000717128:Reln protein, mouse