|  Help  |  About  |  Contact Us

Publication : Developmental expression patterns of alpha1H T-type Ca2+ channels during spermatogenesis and organogenesis in mice.

First Author  Son WY Year  2002
Journal  Dev Growth Differ Volume  44
Issue  3 Pages  181-90
PubMed ID  12060068 Mgi Jnum  J:80260
Mgi Id  MGI:2445598 Doi  10.1046/j.1440-169x.2002.00633.x
Citation  Son WY, et al. (2002) Developmental expression patterns of alpha1H T-type Ca2+ channels during spermatogenesis and organogenesis in mice. Dev Growth Differ 44(3):181-90
abstractText  The objectives of the present study were to investigate the expression patterns of T-type Ca2+ channel mRNA during spermatogenesis and organogenesis in mice. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to identify the subtypes of calcium channels present in the round spermatids isolated from mouse testes by flow cytometry. Transcripts of L-type (alpha1D), non-L-type (alpha1E) and T-type Ca2+ channels were detected in round spermatids. Analysis of PCR products of T-type Ca2+ channels indicated that only alpha1H subunits were detected in round spermatids. The appearance and differential distribution of alpha1H T-type Ca2+ channel mRNA during mouse spermatogenesis and postimplantation embryogenesis (embryonic (E) days E9, E12, E15) were investigated by in situ hybridization with digoxigenin-labeled RNA probes coupled with alkaline phosphatase detection. In testes from adult and immature mice (postnatal 2 and 3 weeks), alpha1H T-type Ca2+ channel mRNA was expressed in all developing germ cells and sertoli cells. On E9 and E12, tissues of the central nervous system, such as the telencephalon, expressed alpha1H T-type Ca2+ channel mRNA. On E15, signals were detected throughout all organs of the embryo. These findings indicate that the expression of alpha1H T-type Ca2+ channels is spatio-temporally regulated during spermatogenesis and organogenesis.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

6 Bio Entities

Trail: Publication

0 Expression