Density-induced social stress alters oxytocin and vasopressin activities in the brain of a small rodent species

It is known that social stress could alter oxytocin(OT)and arginine-vasopressin(AVP)expression in specific regions of brains which regulate the aggressive behavior of small rodents,but the effects of density-induced social stress are still unknown.Brandt’s voles(Lasiopodomys brandtii)are small herbivores in the grassland of China,but the underlying neurological mechanism of population regulation is still unknown.We tested the effects of housing density of Brandt’s voles on OT/AVP system with physical contact(allowing aggression)and without physical contact(not allowing aggression)under laboratory conditions.Then,we tested the effects of paired-aggression(no density effect)of Brandt’s voles on OT/AVP system under laboratory conditions.We hypothesized that high density would increase aggression among animals which would then increase AVP but reduce OT in brains of animals.Our results showed that high housing density induced more aggressive behavior.We found high-densityinduced social stress(with or without physical contact)and direct aggression significantly increased expression of mRNA and protein of AVP and its receptor,but decreased expression of mRNA and protein of OT and its receptor in specific brain regions of voles.The results suggest that density-dependent change of OT/AVP systems may play a significant role in the population regulation of small rodents by altering density-dependent aggressive behavior.

Galectin-7 overexpression destroys airway epithelial barrier in transgenic mice

When the integrity of airway epithelium is destroyed,the ordered airway barrier no longer exists and increases sensitivity to viral infections and allergens,leading to the occurrence of airway inflammation such as asthma.Here,we found that galectin-7 transgenic(+)mice exhibited abnormal airway structures as embryos and after birth.These abnormalities included absent or substantially reduced pseudostratified columnar ciliated epithelium and increased monolayer cells with irregular arrangement and widening of intercellular spaces.Moreover,airway tissue from galectin-7 transgenic(+)mice showed evidence of impaired cell–cell junctions and decreased expression of zonula occludens-1(ZO-1)and E-cadherin.When treated with respiratory syncytial virus(RSV)or ovalbumin(OVA),galectin-7 transgenic(+)mice developed substantially increased bronchial epithelial detachment and apoptosis,airway smooth muscle and basement membrane thickening,and enhanced airway responsiveness.We found that Galectin-7 localized in the cytoplasm and nucleus of bronchial epithelial cells,and that increased apoptosis was mediated through mitochondrial release of cytochrome c and upregulated JNK1 activation and expression of caspase-3 in galectin-7 Tg(+)mice.These findings suggested that Galectin-7 causes airway structural defects and destroys airway epithelium barrier,which predispose the airways to RSV or OVA-induced epithelial apoptosis,injury,and other asthma responses.