Oral Presentation The International Congress of Neuroendocrinology 2014

The monogamous male brain (#91)

Zuoxin Wang 1
  1. Department of Psychology and Program in Neuroscience, Florida State University, Tallahassee, FL, United States

The socially monogamous male prairie vole (Microtus ochrogaster) displays mating-induced pair bonding, demonstrated by a preference for a familiar partner versus a conspecific stranger (partner preference) and aggression toward strangers (selective aggression).  In a study to examine dopamine (DA) regulation of pair bonding, we found that mating induced DA release in the nucleus accumbens (NAcc).  Intra-NAcc activation of DA D2-type (D2R), but not D1-type (D1R), receptors facilitated partner preference formation, whereas the blockade of D2R, but not D1R, inhibited such preference induced by mating or by D2R activation.  Furthermore, two weeks of pair bonding resulted in an increased level of D1R expression in the NAcc in males that displayed selective aggression. Blockade of D1R in the NAcc decreased selective aggression.  These data demonstrate that NAcc DA regulates pair bond formation and maintenance in a receptor-specific manner.

In another study to develop the prairie vole model for the examination of social- and drug-reward interactions, we found that amphetamine (AMPH) is rewarding to male prairie voles, as 3 days of AMPH conditioning dose-dependently induced conditioned place preferences (CPP).  This process is mediated by NAcc D1R.  We also found that such AMPH exposure impaired mating-induced pair bonding and elevated D1R, but not D2R, expression in the NAcc. In addition, blockade of NAcc D1R rescued mating-induced pair bonding in AMPH-treated male voles, implicating the role of NAcc D1R in AMPH impairment of pair bonding. 

Together, our data suggest that NAcc DA mediates social bonding and AMPH reward in a receptor-specific manner, and the socially monogamous prairie voles can be a useful model to examine social- and drug-reward interactions and their underlying neural mechanisms.  (Supported by NIH grants DAR01-019627 and MHR01-058616)