Studies on aggression represent one of the oldest areas of scientific inquiry; however, we still know very little about the neural mechanisms controlling aggression. Developing a better understanding of these neural mechanisms is critical because aggression plays a fundamental role in the formation and maintenance of stable social relationships in many species. Social experience has profound effects on determining an individual's aggressiveness and to understand the mechanisms controlling aggression we must understand how social experience interacts with neural mechanisms and with naturally occurring fluctuations in hormones that influence aggression. This project will examine how competitive and non-competitive social experience interact with the male hormone testosterone to alter aggressiveness. This project will go on to determine whether social experience and testosterone alter aggressiveness by altering the efficacy of a neurochemical signal called arginine-vasopressin (AVP) to influence aggression by its actions in specific areas of the brain. We believe that the data generated by this project will provide critical new insights into the basic principles that govern how neural and endocrine mechanisms control complex social behaviors. This research project will provide opportunities for undergraduates, graduate students and postdocs to be trained in basic neurobiological research.
This project investigated the neurobiological mechanisms that are responsible for social behavior with a special emphasis on competitive behavior and social communication. Studies in males found that social interactions are rewarding even in males that lose competitions. Perhaps not surprisingly social dominance increases the reward value of those interactions. GABA, the primary inhibitory neurotransmitter in the brain, was found to increase aggression in males when injected into the lateral septum regardless of their prior social experience. Other studies in males found that oxytocin (OT) can stimulate social communication by acting not on its own OT receptors, but rather by its action on the primary brain receptor for arginine-vasopression (AVP). We also conducted a series of studies that compared the neurobiogical mechanisms underlying social behavior in females with that previously identified in males. AVP was found to reduce aggression in females and serotonin was found to increase aggression following its injection into the anterior hypothalamus. Surprisingly, the effects of these neurochemicals in females are opposite to their effects on aggression previously found in males. Additional studies examined the seasonal changes that occur in aggression. Females housed in "winter-like" short photoperiods were found to be more aggressive than hamsters housed in "summer-like" long photoperiods. The underlying cause of the seasonal changes in aggression is the ability of short photoperiod to render females insensitive to the aggression-reducing effects of ovarian hormones. Taken together, the data obtained in this project provide important new insights into how social behavior is regulated in both males and females. Last Modified: 09/18/2014 Submitted by: Elliott Albers Missing papers from last submission: Albers, H.E. The regulation of social recognition, social communication and aggression: vasopressin in the social behavior neural network. Horm Behav 2012, 61:283-92. Gil, M., Nguyen, N.T., McDonald, M. and Albers, H.E. Social Reward: interactions with social status, social communication, aggression, and associated neural activation in the ventral tegmental area. Eur J Neurosci 2013, 38:2308-18.
