As vasopressin and its G-protein-coupled receptor (V1(a)R) have find more been shown to affect the outcome of brain edema, we have investigated the regulatory interaction between AQP4 and V1(a)R by heterologous expression in Xenopus laevis oocytes. The water permeability of AQP4/V1(a)R-expressing oocytes was reduced in a vasopressin-dependent manner, as a result of V1(a)R-dependent internalization of AQP4.

Vasopressin-dependent internalization was not observed in AQP9/V1(a)R-expressing oocytes. The regulatory interaction between AQP4 and V1(a)R involves protein kinase C (PKC) activation and is reduced upon mutation of Ser(180) on AQP4 to an alanine. Thus, the present study demonstrates at the molecular level a functional link between the vasopressin receptor V1(a)R and AQP4. This functional interaction between AQP4 and V1(a)R may prove to be a potential therapeutic target in the prevention and treatment of brain edema. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Negative exchanges in social relationships have traditionally been studied as having negative consequences. This study explored whether they might have positive effects for relationship closeness. The sample included 351 adults, aged between 18 and 91 years, residing in Hong Kong, China. Closeness of social partners to the participants

was measured by the Social Convoy Questionnaire, and the levels of negative exchanges and social support from each social partner were assessed. Multilevel analyses revealed that more negative exchanges were associated with a more positive change in closeness over a 2-year period, even after statistically PLX-4720 molecular weight controlling for social support and sociostructural characteristics of the participant and the social partner. Findings check details extended our knowledge on the positive effects of negative exchanges and their moderating conditions.”
“The human natural killer-1 (HNK-1) glyco-epitope possesses a unique structural

feature, a sulfated glucuronic acid attached to lactosamine on the non-reducing termini of glycans. The expression of HNK-1 is temporally and spatially regulated by glucuronyltransferase (GlcAT-P) in the brain. Our previous report showed that mice lacking GlcAT-P almost completely lost HNK-1 expression in the brain and exhibited reduced long-term potentiation (LTP) at hippocampal CA1 synapses. GlcAT-P-deficient mice also showed impaired hippocampus-dependent spatial learning. Although HNK-1 plays an essential role in synaptic plasticity and memory formation, it remains unclear how HNK-1 regulates these functions. In this study, we showed that loss of the HNK-1 epitope resulted in an increase of filopodium-like immature spines and a decrease of mushroom-like mature spines in both the early postnatal mouse hippocampus and cultured hippocampal neurons. However, HNK-1 had no influence on spine density or filopodium formation.