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Orexinergic neurons modulate REMS by influencing locus coeruleus neurons
Author(s) -
Ajeet Kumar,
Himanshu K. Mishra,
Priyanka Dwivedi,
R. Jamuna,
Subramaniam,
H. K. Srivastava,
B. N. Mallick
Publication year - 2012
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2012.03.245
Subject(s) - locus coeruleus , neuroscience , citation , psychology , cognitive science , library science , computer science , nucleus
a compensatory increase at E18. To resolve whether this delay in neurogenesis is due to defect in differentiation from progenitors, double labeling with the mitotic marker BrdU and cell cycle marker Ki67 was performed at E16, and cell cycle quitting fraction was analyzed by flow cytometry and 5 folds decrease was seen under hypothyroidism. It could be either from diminished mitotic pool of ventricular zone (VZ) resident apical progenitors or subventricular zone (SVZ) resident intermediate progenitor cells (IPCs). Mapping of mitotic figures by p-Histone3 immunostaining revealed a significant reduction in the mitotic progenitors in intermediate zone and increase in the VZ progenitors under hypothyroidism, indicating loss of proliferating IPCs. This was further confirmed with the significant decrease in IPCs specific marker Tbr2 under hypothyroidism. The loss of indirect neurogenesis by IPCs was also evident in the reduction of telencephalic thickness under maternal hypothyroidism. Cultured neuronal progenitors showed expression TH transporter MCT8, De-iodinase-II and TH receptor TR 1 indicating that IPCs can metabolize maternal TH and explains their regulation by altered TH status during development. Taken, together we describe direct regulation of neurogenesis by maternal TH as seen by diminished pool of IPCs during development under hypothyroidism.