本期封面所示為進(jìn)行社會性游戲的巢鼠（禾鼠）,。人們此前一直不知道社會獎賞編碼背后的神經(jīng)機(jī)制，盡管需要增強(qiáng)適應(yīng)性社會互動來在整個(gè)演化過程中始終保持這樣的行為,。Robert Malenka及同事在本文中報(bào)告說，在小鼠伏隔核中,，肽激素“后葉催產(chǎn)素”對于向“中等多棘神經(jīng)元”上的激發(fā)性傳輸?shù)纳鐣栽鰪?qiáng)和一種形式的突觸前長期抑制來說都是所必需的,。如果“后葉催產(chǎn)素”受體被特意從來自“背縫神經(jīng)核”（腦中5-羥色胺的主要來源）的輸入中刪除的話，這種社會性增強(qiáng)就會被中斷,；通過阻斷伏隔核中的5-羥色胺受體,，這種社會性增強(qiáng)也會被中斷。“后葉催產(chǎn)素”和5-羥色胺系統(tǒng)之間這種協(xié)調(diào)的活性,，為編碼社會性增強(qiáng)提供了一個(gè)可能的機(jī)制,，也為進(jìn)一步研究社會功能失調(diào)的神經(jīng)機(jī)制提供了目標(biāo)。封面：Jean-Louis Klein & Marie-Luce Hubert,。（生物谷 Bioon.com）
生物谷推薦的英文摘要
Nature doi:10.1038/nature12518
Social reward requires coordinated activity of nucleus accumbens oxytocin and serotonin
Gül Dölen, Ayeh Darvishzadeh, Kee Wui Huang & Robert C. Malenka
Social behaviours in species as diverse as honey bees and humans promote group survival but often come at some cost to the individual. Although reinforcement of adaptive social interactions is ostensibly required for the evolutionary persistence of these behaviours, the neural mechanisms by which social reward is encoded by the brain are largely unknown. Here we demonstrate that in mice oxytocin acts as a social reinforcement signal within the nucleus accumbens core, where it elicits a presynaptically expressed long-term depression of excitatory synaptic transmission in medium spiny neurons. Although the nucleus accumbens receives oxytocin-receptor-containing inputs from several brain regions, genetic deletion of these receptors specifically from dorsal raphe nucleus, which provides serotonergic (5-hydroxytryptamine; 5-HT) innervation to the nucleus accumbens, abolishes the reinforcing properties of social interaction. Furthermore, oxytocin-induced synaptic plasticity requires activation of nucleus accumbens 5-HT1B receptors, the blockade of which prevents social reward. These results demonstrate that the rewarding properties of social interaction in mice require the coordinated activity of oxytocin and 5-HT in the nucleus accumbens, a mechanistic insight with implications for understanding the pathogenesis of social dysfunction in neuropsychiatric disorders such as autism.
