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.
