This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Voles provide an excellent animal model for investigating the molecular, cellular and neural mechanisms underlying affiliative behavior and social attachment. Pharmacological studies have demonstrated that vasopressin plays an important role in pair bond formation in the monogamous prairie vole. Comparisons of the vasopressin system between prairie voles and non-monogamous vole species demonstrate that species differences in the promoter of the V1a receptor (V1aR) gene and the neuroanatomical pattern of expression of the gene may be responsible for species differences in social behavior. Prairie voles express high levels of V1aR gene expression in the ventral pallidum, laterodorsal thalamus and medial amygdala, compared to non-monogamous montane and meadow voles. Using transgenic mice, we have demonstrated that neuroanatomical distribution of V1aR does influence the behavioral response to vasopressin. In addition, using an adeno-associated viral vector, we have demonstrated that over-expressing the V1a receptor in the ventral pallidum of male prairie voles leads to increased affiliative behavior and facilitates the formation of a pairbond. The ventral pallidum is a major component of the mesolimbic reward pathway, and has been identified as a site of action for drugs of abuse such as cocaine and amphetamine. Other non-related monogamous species, including Peromyscous californicus and the common marmoset, also have high levels of V1aR in the ventral pallidum compared to non-monogamous species such as P. leucopus and rhesus macaques. In this application, we propose to: 1) Investigate the relationship between V1aR gene structure, V1aR gene expression and social behavior. 2) Use site specific injections of V1aR antagonist or viral vector gene transfer to determine whether V1aR activation in the ventral pallidum is necessary for pair bonding and 3) Use immunocytochemistry and tract tracing to examine the projections of the V1a receptor-containing neurons of the ventral pallidum. The results from experiments described in this proposal may provide information useful in understanding the biological basis of psychiatric diseases characterized by deficits in social behavior.
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