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Aberrant nest building and prolactin secretion in vitamin D receptor mutant mice
- Source :
- The Journal of steroid biochemistry and molecular biology. 104(3-5)
- Publication Year :
- 2007
-
Abstract
- 1Alpha,25(OH)2D3, the hormonal form of vitamin D, is a neuroactive seco-steroid hormone with multiple functions in the brain. Most of these effects are mediated through the nuclear vitamin D receptor (VDR), widely distributed in the central nervous system. Our earlier studies showed that mutant mice lacking functional VDR have specific behavioural abnormalities, including anxiety and aberrant maternal behaviour, which may be hormonally regulated. Here we describe impaired nest building behaviour in VDR mutant mice. Since prolactin plays a key role in the regulation of nest building in both sexes, we also examine whether VDR mutant mice have altered prolactin levels. Overall, serum prolactin levels were increased in VDR mutant mice, accompanied by marked impairments in their nest building activity. In contrast, there were no differences in prolactin mRNA expression levels between wildtype control mice and VDR mutant mice. Collectively, these data suggest that partial genetic ablation of VDR affects prolactin system in mice, and that altered serum prolactin levels in VDR mutants may underlie some of their behavioural abnormalities, such as impaired nest building.
- Subjects :
- Male
medicine.medical_specialty
Endocrinology, Diabetes and Metabolism
medicine.medical_treatment
Clinical Biochemistry
Mutant
Biology
Biochemistry
Calcitriol receptor
Nesting Behavior
Mice
Endocrinology
Internal medicine
medicine
Animals
RNA, Messenger
Receptor
Molecular Biology
Wild type
Cell Biology
Prolactin
Mice, Mutant Strains
Steroid hormone
Nuclear receptor
Molecular Medicine
Receptors, Calcitriol
lipids (amino acids, peptides, and proteins)
Hormone
Subjects
Details
- ISSN :
- 09600760
- Volume :
- 104
- Issue :
- 3-5
- Database :
- OpenAIRE
- Journal :
- The Journal of steroid biochemistry and molecular biology
- Accession number :
- edsair.doi.dedup.....7e1dac8a224ae7a01c961aed04845fe3