Thomas R. Insel, Ph.D.
Director, National Institute of Mental Health
March 22, 2004
Social Neuroscience: From Genes to Behavior
One of the most challenging questions for our understanding of the brain is how this complex organ of a few billion cells manages complex functions such as language, emotion, and consciousness. This presentation takes on the seemingly impossible task of trying to understand the brain mechanisms for complex behavior, specifically social attachment (which, in humans, we call "love"). This task becomes tractable because of two insights. First, there are many mammals (besides humans), which form long-term social attachments. Our studies have focused on prairie voles, a monogamous rodent. The second insight is that a family of neuropeptides, including oxytocin and vasopressin, seems to have an important role in social behavior across evolution.
Vasopressin and oxytocin appear to be critical for the development of a long-term selective social bond in prairie voles. Under natural conditions, prairie voles form bonds only after mating. If oxytocin or vasopressin is given in the absence of mating, the voles will bond. More important, if prairie voles mate but are treated with a blocker of oxytocin or vasopressin, they fail to bond. Thus, it appears that these neuropeptides, normally released with mating, are necessary and sufficient for pair bonding. What is intriguing is that these neuropeptides have no such effect in other species of voles that are not monogamous. Prairie voles, as well as other monogamous species, have a unique distribution of brain receptors for oxytocin and vasopressin, such that these neuropeptides can influence reward pathways in the brains of monogamous species. The mechanism for these striking species differences in receptor distribution is not entirely clear, but may be related to a variation in the sequence of the regulatory part of the genes for these receptors. Engineering the mouse genome to induce a prairie-vole like pattern of receptors results in an increase in social behavior in response to vasopressin.
One implication of these results involves autism, a neurodevelopment disorder characterized by a reduction in social behavior and abnormal social attachment. There are reports of reduced oxytocin in children with autism. Perhaps more important is a recent finding that the same genetic region which discriminates monogamous from non-monogamous voles also appears to show variation in the human genome and that one version of this region is transmitted at a high rate in children with autism. We do not know yet whether the autistic brain has an altered distribution of vasopressin or oxytocin receptors. Nevertheless, a principle elucidated from the vole studies-that the confluence of oxytocin or vasopressin circuits with the brain's reward pathways is critical for social attachment- deserves careful study in autism.