Postnatal ontogeny of the transcription factor Lmx1b in the mouse central nervous system

被引:57
作者
Dai, Jin-Xia
Hu, Ze-Lan
Shi, Ming
Guo, Chao
Ding, Yu-Qiang [1 ]
机构
[1] Chinese Acad Sci, Inst Neurosci, Shanghai 200031, Peoples R China
关键词
localization; brain; Tlx3; postanatal development; in situ hybridization; immunohistochemistry;
D O I
10.1002/cne.21759
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The expression profile of Lim homeodomain transcription factor Lmx1b in the mouse brain was investigated at different postnatal stages by immunohistochemistry and in situ hybridization. At postnatal day (P) 7, many Lmx1b-expressing neurons were found in the posterior hypothalamic area, supramammillary nucleus, ventral premammillary nucleus, and subthalamic nucleus. In the midbrain, numerous Lmx1b-expressing neurons were present in the substantia nigra pars compacta and ventral tegmental area. In the hindbrain, Lmx1b-expressing neurons were primarily observed in the raphe nuclei, parabrachial nuclei, principal sensory trigeminal nucleus, nucleus of the solitary tract, and laminae I-II of the medullary dorsal horn as well as spinal dorsal horn. Although expression levels diminished as postnatal life progressed, persistent expression throughout the first year of life was observed in many of these regions. In contrast, Lmx1b was present in a few brain regions (e.g., principal sensory trigeminal nucleus) only in early life with expression expiring by P60. Lmx1b was observed in dopaminergic neurons in the midbrain and serotonergic neurons in the hindbrain, as determined by double labeling with specific markers. In addition, we found that Lmx1b-expressing neurons are got GABAergic, and Lmx1b was colocalized with T1x3 in the parabrachial nuclei, principal sensory trigeminal nucleus, nucleus of the solitary tract. as well as the medullary and spinal dorsal horns, suggesting that Lmx1b-expressing cells in these areas are excitatory neurons. Our data suggest that Lmx1b is involved in the postnatal maturation of certain types of neurons and maintenance of their normal functions in the adult brain.
引用
收藏
页码:341 / 355
页数:15
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