A series of classic studies have shown that in Prairie Voles two neuropeptides, oxytocin and vasopressin, are primary modulators of pair-bond formation and parental behaviors. Genetic manipulations have been able to switch male behaviors between pair-bonding and promiscuous, and correlations between similar behaviors in human males and their genetic variations have been found. Recently Cushing et al. have made another observation on male voles which one expects will also be carried over to human males: Prosocial behavior correlates with a low density of estrogen receptors in the lateral amygdala, and genetic manipulations which increase the number of these receptors decrease pair-bonding and prosocial behaviors. It will be interesting to follow efforts to translate these findings to human social bonding, especially in relation to neuropsychiatric disorders characterized by an inability to form normal social bonds, such as autism. Here is their abstract:
Studies using estrogen receptor (ER) knock-out mice indicate that ER masculinizes male behavior. Recent studies of ER and male prosocial behavior have shown an inverse relationship between ER expression in regions of the brain that regulate social behavior, including the medial amygdala (MeA), and the expression of male prosocial behavior. These studies have lead to the hypothesis that low levels of ER are necessary to "permit" the expression of high levels of male prosocial behavior. To test this, viral vectors were used to enhance ER in male prairie voles (Microtus ochrogaster), which display high levels of prosocial behavior and low levels of MeA ER. Adult male prairie voles were transfected with ER in the MeA (MeA-ER) or the caudate–putamen (ER control) or luciferase (MeA-site-specific control), and 3 weeks later tested for spontaneous alloparental behavior and partner preference. Enhancing ER in the MeA altered/reduced male prosocial behavior. Only one-third of MeA-ER males, compared with all control males, were alloparental. MeA-ER males also displayed a significant preference for a novel female. This is a critical finding because the manipulations of neuropeptides, oxytocin and vasopressin, can inhibit the formation of a partner preference, but do not lead to the formation of a preference for a novel female. The results support the hypothesis that low levels of ER are necessary for high levels of male prosocial behavior, and provide the first direct evidence that site-specific ER expression plays a critical role in the expression of male prosocial behavior.