1. Expression of the LIM-homeodomain gene Lmx1a in the postnatal mouse central nervous system.
- Author
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Zou HL, Su CJ, Shi M, Zhao GY, Li ZY, Guo C, and Ding YQ
- Subjects
- Animals, Brain growth & development, Cell Count, Gene Expression, Immunohistochemistry, In Situ Hybridization, LIM-Homeodomain Proteins, Mice, Mice, Inbred C57BL, RNA, Messenger genetics, RNA, Messenger metabolism, Spinal Cord growth & development, Transcription Factors, Tyrosine 3-Monooxygenase metabolism, Brain metabolism, Homeodomain Proteins genetics, Homeodomain Proteins metabolism, Spinal Cord metabolism
- Abstract
The LIM-homeodomain transcription factor Lmx1a plays critical roles in roof plate formation as well as in the cell fate determination of midbrain dopaminergic neurons during embryonic development, but its function in the adult brain remains unknown. In the present study, as the first step in exploring its function in adult brain, we examined the expression of Lmx1a in the mouse central nervous system (CNS) from birth to adulthood by in situ hybridization. Lmx1a was expressed at high levels in the posterior hypothalamic area, supremammillary nucleus, ventral premammillary nucleus, subthalamic nucleus, ventral tegmental area, compact part of the substantia nigra and parabrachial nucleus from birth to adulthood, and co-localized with its paralogue Lmx1b in these regions. On the other hand, Lmx1a expression in the cochlear nuclei, medial cerebellar nucleus and superior vestibular nucleus was only observed until postnatal day (P) 30 and showed no colocalization with Lmx1b. Lmx1a-expressing neurons in the ventral midbrain were dopaminergic as evidenced by co-expression with tyrosine hydroxylase in these regions. Furthermore, Lmx1a expression was also found in the choroid plexuses and ependymal cells, although its expression was only detected during the first two postnatal weeks. These results suggest that Lmx1a may be involved in postnatal development as well as in maintenance of some aspects of normal brain function.
- Published
- 2009
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