For further testing therefore 0.5 mu g i.c.v. was used. Propranolol and atropine fully blocked the NmU-induced anxiolytic action, while haloperidol, phenoxybenzamine and nitro-L-arginine were ineffective. The results suggest that beta-adrenergic and cholinergic mechanisms are involved in the anxiolytic action of NmU. (C) 2013 Elsevier B.V. All rights reserved.”
“Background: Granulosa cells play a key role in folliculogenesis
and female reproduction. Our previous study demonstrated that water channel aquaporin- 8 (AQP8) is expressed in mouse follicular granulosa cells and is an important determinant of granulosa cell apoptosis and follicular maturation. More roles of AQP8 in folliculogenesis remain to be determined.
Findings: The present study reports the increased occurrence Verubecestat manufacturer of multi-oocyte follicles (MOFs) in ovaries of AQP8 knockout mice.
The MOFs in AQP8-deficient ovaries contained two or three oocytes, and distributed at various follicle stages including primary (12.5%), secondary (50%), antral (18.8%) and atretic PF-02341066 in vitro (18.8%) follicles in 5-week ovaries. The MOF is occasionally seen in wild-type ovary only in primary and secondary follicles. The number of MOFs in AQP8-deficient ovary reduced with age (26.7 +/- 5.2 per ovary at 5 weeks old, 14 +/- 5.5 at 10 weeks old, and 3.3 +/- 5.1 at 20 weeks old). mRNA expression of AQP5, AQP7, AQP8, AQP11 and AQP12 was detected in neonatal mouse ovaries and in granulosa cells in 4 week old mouse ovaries. The expression of AQP7, AQP11 and AQP12 mRNAs are decreased significantly in neonatal AQP8-deficient ovaries, whereas AQP5 mRNA expression remains unchanged.
Conclusions: The emergence of MOFs is associated with AQP8 deficiency. The study suggested the involvement of AQP8 in the formation of follicles and provided new AG-120 insight into the molecular mechanisms of folliculogenesis.”
“The role of specific gut microbes in shaping body composition remains unclear. We transplanted fecal microbiota
from adult female twin pairs discordant for obesity into germ-free mice fed low-fat mouse chow, as well as diets representing different levels of saturated fat and fruit and vegetable consumption typical of the U.S. diet. Increased total body and fat mass, as well as obesity-associated metabolic phenotypes, were transmissible with uncultured fecal communities and with their corresponding fecal bacterial culture collections. Cohousing mice harboring an obese twin’s microbiota (Ob) with mice containing the lean co-twin’s microbiota (Ln) prevented the development of increased body mass and obesity-associated metabolic phenotypes in Ob cage mates. Rescue correlated with invasion of specific members of Bacteroidetes from the Ln microbiota into Ob microbiota and was diet-dependent. These findings reveal transmissible, rapid, and modifiable effects of diet-by-microbiota interactions.