|  Help  |  About  |  Contact Us

Publication : In vitro fertilization and microinsemination with round spermatids for propagation of nephrotic genes in mice.

First Author  Ogura A Year  1996
Journal  Theriogenology Volume  45
Issue  6 Pages  1141-9
PubMed ID  16727871 Mgi Jnum  J:281013
Mgi Id  MGI:6377185 Doi  10.1016/0093-691x(96)00070-2
Citation  Ogura A, et al. (1996) In vitro fertilization and microinsemination with round spermatids for propagation of nephrotic genes in mice. Theriogenology 45(6):1141-9
abstractText  The ICGN is an inbred strain of mice with a hereditary nephrotic syndrome of an unknown cause. The disease progresses to renal failure, resulting in the deterioration of the systemic condition and in a drastic reduction of reproductive capacity. The present study was undertaken to determine if in vitro fertilization (IVF) and microinsemination using round spermatids could ameliorate the reduced fertility of ICGN mice. Mature oocytes (9.4 +/- 1.1 per mouse) were obtained from PMSG/hCG-primed females 2 to 5 mo of age. When spermatozoa from males aged 3 to 4 mo was used for IVF, a high fertilization rate (82.6%) was achieved and a high rate of embryos developed into blastocysts (92.6%). When spermatozoa from males aged 5 to 7 mo was used, the rates of fertilization and development to blastocysts were significantly lower (63.9 and 47.1%, respectively; P < 0.001). However, the production rate of offspring after embryo transfer was satisfactory irrespective of the age of males (59.1%). When males older than 9 mo were used, no fertilization was achieved due to the very poor motility of the spermatozoa. Microinsemination techniques with round spermatids (electrofusion and intracytoplasmic injection) resulted in the production of normal offspring from the older males, including one azoospermic case. These findings indicate that a conventional IVF technique and microinsemination using round spermatids can be used for propagating mutant genes which cause poor reproductive ability in mice.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

0 Bio Entities

0 Expression