Sex-dependent effects of pair bond interruption on anxiety- and depression-like behaviors in adult mandarin voles.

Stable and positive social bonds are pretty vital to the development of animals. Instability and disruptions of social bonds, such as maternal separation and social isolation, always produce disastrous influence on physiology, neuroendocrine and behaviors. Pair bond is one of the most important social bonds in adulthood. But the different effects of pair bond interruption between males and females are rarely studied. In the present study, the monogamous mandarin voles (Microtus mandarinus) were used to confirm the time window of pair bond formation. After that, voles were separated from their partner for 1 or 2 weeks. Then anxiety- and depression-like behaviors were investigated by using open field test, light-dark box test, tail suspension test and forced swimming test, respectively. The results showed that: (1) cohabitation for 5 days is sufficient and necessary for mandarin voles to form pair bond; (2) loss of partner is always crucial for the effects of pair bond interruption, while social isolation works in certain behavioral tests.; (3) pair bond interruption for 2 weeks significantly increased the level of anxiety and depression in adult males, but not female mandarin voles. Overall, this research suggested that loss of partner plays a key role in pair bond interruption in male mandarin voles.

Age-dependent decline of DNA repair activity for oxidative lesions in rat brain mitochondria.

Endogenous oxidative damage to brain mitochondrial DNA and mitochondrial dysfunction are contributing factors in aging and in the pathogenesis of a number of neurodegenerative diseases. In this study, we characterized the regulation of base-excision-repair (BER) activity, the predominant repair mechanism for oxidative DNA lesions, in brain mitochondria as the function of age. Mitochondrial protein extracts were prepared from rat cerebral cortices at the ages of embryonic day 17 (E17) or postnatal 1-, 2-, and 3-weeks, or 5- and 30-months. The total BER activity and the activity of essential BER enzymes were examined in mitochondria using in vitro DNA repair assay employing specific repair substrates. Mitochondrial BER activity showed marked age-dependent declines in the brain. The levels of overall BER activity were highest at E17, gradually decreased thereafter, and reached to the lowest at the age of 30-month ( approximately 80% reduction). The decline of overall BER activity with age was attributed to the decreased expression of repair enzymes such as 8-OHdG glycosylase and DNA polymerase-gamma and, consequently, the reduced activity at the steps of lesion-base incision, DNA repair synthesis and DNA ligation in the BER pathway. These results strongly suggest that the decline in BER activity may be an important mechanism contributing to the age-dependent accumulation of oxidative DNA lesions in brain mitochondria.