<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Dai, L.</style></author><author><style face="normal" font="default" size="100%">Carter, C. S.</style></author><author><style face="normal" font="default" size="100%">Ying, J.</style></author><author><style face="normal" font="default" size="100%">Bellugi, U.</style></author><author><style face="normal" font="default" size="100%">Pournajafi-Nazarloo, H.</style></author><author><style face="normal" font="default" size="100%">Korenberg, J. R.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Oxytocin and vasopressin are dysregulated in Williams Syndrome, a genetic disorder affecting social behavior</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS One</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">*Social Behavior</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxytocin/*physiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Vasopressins/*physiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Williams Syndrome/*physiopathology</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22719898</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">6</style></number><volume><style face="normal" font="default" size="100%">7</style></volume><pages><style face="normal" font="default" size="100%">e38513</style></pages><isbn><style face="normal" font="default" size="100%">1932-6203 (Electronic)&lt;br/&gt;1932-6203 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The molecular and neural mechanisms regulating human social-emotional behaviors are fundamentally important but largely unknown; unraveling these requires a genetic systems neuroscience analysis of human models. Williams Syndrome (WS), a condition caused by deletion of ~28 genes, is associated with a gregarious personality, strong drive to approach strangers, difficult peer interactions, and attraction to music. WS provides a unique opportunity to identify endogenous human gene-behavior mechanisms. Social neuropeptides including oxytocin (OT) and arginine vasopressin (AVP) regulate reproductive and social behaviors in mammals, and we reasoned that these might mediate the features of WS. Here we established blood levels of OT and AVP in WS and controls at baseline, and at multiple timepoints following a positive emotional intervention (music), and a negative physical stressor (cold). We also related these levels to standardized indices of social behavior. Results revealed significantly higher median levels of OT in WS versus controls at baseline, with a less marked increase in AVP. Further, in WS, OT and AVP increased in response to music and to cold, with greater variability and an amplified peak release compared to controls. In WS, baseline OT but not AVP, was correlated positively with approach, but negatively with adaptive social behaviors. These results indicate that WS deleted genes perturb hypothalamic-pituitary release not only of OT but also of AVP, implicating more complex neuropeptide circuitry for WS features and providing evidence for their roles in endogenous regulation of human social behavior. The data suggest a possible biological basis for amygdalar involvement, for increased anxiety, and for the paradox of increased approach but poor social relationships in WS. They also offer insight for translating genetic and neuroendocrine knowledge into treatments for disorders of social behavior.</style></abstract><accession-num><style face="normal" font="default" size="100%">22719898</style></accession-num><notes><style face="normal" font="default" size="100%">Dai, Li&lt;br/&gt;Carter, C Sue&lt;br/&gt;Ying, Jian&lt;br/&gt;Bellugi, Ursula&lt;br/&gt;Pournajafi-Nazarloo, Hossein&lt;br/&gt;Korenberg, Julie R&lt;br/&gt;eng&lt;br/&gt;MH072935/MH/NIMH NIH HHS/&lt;br/&gt;P01 HD033113/HD/NICHD NIH HHS/&lt;br/&gt;P01 HD33113/HD/NICHD NIH HHS/&lt;br/&gt;Research Support, N.I.H., Extramural&lt;br/&gt;2012/06/22 06:00&lt;br/&gt;PLoS One. 2012;7(6):e38513. doi: 10.1371/journal.pone.0038513. Epub 2012 Jun 12.</style></notes><custom2><style face="normal" font="default" size="100%">PMC3373592</style></custom2><auth-address><style face="normal" font="default" size="100%">Center for Integrated Neuroscience and Human Behavior, and Department of Pediatrics, University of Utah, Salt Lake City, Utah, United States of America.</style></auth-address></record></records></xml>