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Submitted on June 28, 2005
Accepted on November 1, 2005
Department of Developmental Biology, Faculty of Medicine, Shimane University, Izumo 693-8501, Japan; Department of Oral and Maxillofacial Surgery, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan; Central Institute for Experimental Animals, Kawasaki 216-0001, Japan; Department of Food Science, Shimane Women's College, Matsue 690-0044, Japan; Department of Genome Sciences, Faculty of Medical Sciences, Kobe University, Graduate School of Medicine, Kobe 650-0017, Japan
* To whom correspondence should be addressed. E-mail: jun{at}med.shimane-u.ac.jp.
Leptin is detected in the sera and leptin receptors are expressed in the cerebrum of mouse embryos, suggesting that leptin plays a role in cerebral development. Compared with the wild-type, leptin-deficient (ob/ob) mice had fewer cells at embryonic day (E) 16 and E18 and had fewer BrdU+ cells at E14 and E16 in the neuroepithelium (NE). Intracerebroventricular leptin injection in E14 ob/ob embryos increased the number of NE cells at E16. In cultured neurosphere cells, leptin treatment increased Hes1 mRNA expression and maintained neural progenitors. Astrocyte differentiation was induced by low-dose (0.1 µg/ml) but not high-dose (1 µg/ml) leptin. High-dose leptin decreased Id mRNA and increased Ngn1 mRNA in neurosphere cells. The NPY mRNA level in the cortical plate was lower in ob/ob than in the wild-type at E16 and E18. These results suggest that leptin maintains neural progenitors and is related to glial and neuronal development in embryos.
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