Edward S. Brodkin, MD

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				Edward S. Brodkin, M.D. Assistant Professor of Psychiatry University of Pennsylvania School of Medicine Center for Neurobiology and Behavior Translational Research Laboratory, Room 2220 125 South 31 st Street Philadelphia, PA 19104-3403 Phone: (215)-746-0118 Fax: (215)-573-2041 ebrodkin@mail.med.upenn.edu www.uphs.upenn.edu/cnb/brodkin.htm www.med.upenn.edu/add/brodkin.shtml Click here for selected publications since Dr. Brodkin's arrival at Penn RESEARCH INTERESTS Neurobiology of social behaviors, including aggressive and affiliative behaviors, studied using genetic analysis in mouse model systems. Neurobiology and genetics of autism spectrum disorders RESEARCH TECHNIQUES Measurement of mouse social behaviors, genetic mapping, quantitative trait locus (QTL) analysis, behavioral and gene expression analysis in single gene mutant mice (e.g. knockouts). RESEARCH SUMMARY Our laboratory uses methods of genetics and genomics to dissect the neurobiological pathways mediating social behaviors, including aggression and sociability (tendency to seek social interaction). Certain neuropsychiatric disorders, including autism and schizophrenia, are characterized by extremely disabling disturbances in social cognition and socioemotional behaviors. Despite its importance, the fundamental biology of these social behaviors is not well understood. Our laboratory is focused on the following major questions of interest: What are the neurobiological mechanisms that underlie the tendency to seek or avoid affiliative social interactions? What are the neurobiological mechanisms that promote or inhibit the initiation of aggressive behaviors? What genes and environmental factors contribute to individual differences in sociability and aggressive behaviors? What genes and environmental factors contribute to the etiology and pathophysiology of “disorders of social relatedness,” e.g. autism spectrum disorders or schizophrenia? Currently, most of our genetic studies of social behaviors use the mouse as a model organism, because of the experimental control that a model organism provides, and because of the many resources available for mouse genetics. These studies may have relevance to human brain and behavior. For virtually every mouse gene, there is a homologous human gene, and vice versa. Moreover, the genetic and neurobiological pathways underlying primitive social behaviors, such as aggression, appear to have been conserved, to some extent, across mammalian evolution. Thus, animal studies may help to identify candidate genes and neurobiological pathways that may be involved autism or other human neuropsychiatric disorders. Previously, in a whole genome scan, we identified quantitative trait loci (QTLs) on chromosome 10 and chromosome X that affect intermale aggressive behaviors in a cross of NZB/B1NJ and A/J inbred mice (Brodkin et al., 2002). Currently, we are fine-mapping these genetic loci by breeding interval-specific congenic strains, and we are sequencing and analyzing positional candidate genes for aggression. We also are using single-gene mutant mice (e.g. knockouts) to dissect pathways that mediate aggressive behaviors. In addition to our work on aggressive behaviors, we have demonstrated differences among inbred mouse strains in sociability, using a social choice behavioral paradigm (Brodkin et al., 2004; Sankoorikal et al 2006). Our studies indicate that the BALB/cJ inbred strain shows reduced sociability and other behavioral and neurobiological traits relevant to autism (Brodkin, 2007). A new set of studies in our laboratory is aimed at elucidating the brain pathways that underlie this reduced sociability of BALB/cJ mice. Also, we have initiated studies of mice with knockouts of autism candidate genes. A neural pathway from the vomeronasal organ to accessory olfactory bulb to medial amygdala to bed nucleus of stria terminalis (BNST) and medial preoptic area (MPOA) is involved in processing social/olfactory/pheromone information and mediating social behaviors in rodents. The amygdala is also thought to play an important role in processing social information in humans. We are studying the role of this pathway in mouse models of aggression and sociability mentioned above. KEY WORDS: social; behavior; affiliation; aggression; attachment; autism; motivation; emotion; genetics; individual differences; complex traits; mouse