Edward Stuart Brodkin, M.D.

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Associate Professor of Psychiatry
Department: Psychiatry
Graduate Group Affiliations

Contact information
Center for Neurobiology and Behavior
Department of Psychiatry
Perelman School of Medicine at the University of Pennsylvania
Translational Research Laboratory, Room 2220
125 South 31st Street
Philadelphia, PA 19104-3403
Office: (215)-746-0118
Fax: (215)-573-2041
A.B. (History of Science)
Harvard University, 1988.
M.D. (Medicine)
Harvard Medical School, 1992.
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Description of Research Expertise


Developmental neurobiology and genetics of social behaviors, including social affiliative and aggressive behaviors, studied primarily in mouse model systems. Neurobiology of social behavior phenotypes in mouse models of autism and schizophrenia spectrum disorders.


social; behavior; affiliation; aggression; autism; schizophrenia; motivation; emotion; genetics; mouse


Measurement of mouse social affiliative behaviors, aggressive behaviors, anxiety-related behaviors, and olfaction; behavioral genetics, genetic mapping, quantitative trait locus (QTL) analysis; behavioral and neurobiological studies of mice with spontaneous or induced mutations of autism- and schizophrenia susceptibility genes; immunohistochemistry; autoradiography; microarray analysis of gene expression; behavioral pharmacology.


Our laboratory is interested in the neurobiological and genetic mechanisms of social behavior development, including the development of social affiliative and aggressive behaviors. Social interactions can have both rewarding and aversive qualities for an individual. The balance between reward and aversion depend upon the context of the interaction, as well as the genetically-shaped temperament and developmental history of the individual. Certain highly heritable neuropsychiatric disorders, including autism and schizophrenia spectrum disorders, are characterized by disabling social withdrawal and disturbances in social cognition. Despite its importance, the fundamental biology of these social behaviors is not well understood, and currently available treatments for these social behavior symptoms are inadequate.

Our studies of the biology 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. For virtually every mouse gene, there is a homologous human gene, and vice versa. Moreover, the genetic and neurobiological pathways underlying basic social behaviors, such as affiliation and aggression, appear to have been conserved, to a substantial extent, across mammalian evolution. Thus, animal studies can help to elucidate neurobiological pathways and mechanisms that are involved in autism, schizophrenia, and other human neuropsychiatric disorders.

Mice and many other mammals rely heavily on olfactory information from conspecifics (pheromones and other odorants) to guide social interactions, whereas humans rely more heavily on visual and auditory information (facial expression and language). However in virtually all mammals, the emotional/motivational significance of this sensory information about the social world is processed, downstream, by various amygdala nuclei, the bed nucleus of stria terminalis (BNST), various hypothalamic nuclei, the nucleus accumbens, and the lateral septum. We are studying the role of these neural circuits in social affiliative and aggressive behaviors, using mouse models.

Our current projects include the following: 1) Studies of the neurobiology of individual differences in social affiliative behaviors, using behavioral, pharmacologic, and genetic methods in inbred mouse strains; 2) studies of the neurobiology of social behavior phenotypes in mice with spontaneous or induced mutations of autism or schizophrenia susceptibility genes; 3) studies of gene-environment (prenatal inflammation) interactions in shaping social behavior development; 4) studies of the neurobiology of candidate genes in a quantitative trait locus that affects aggressive behaviors in mice.

Selected Publications

Fairless A.H., Shah R.Y., Guthrie A.J., Li H., Brodkin E.S.: Deconstructing sociability, an autism-relevant phenotype, in mouse models. The Anatomical Record (Special Issue: “New Concepts in Developing Brain Disorders--Autism”) 294: 1713-1725, 2011.

Dow H.C., Kreibich A.S., Kaercher K.A., Sankoorikal G.M.V., Pauley E.D., Lohoff F.W., Ferraro T.N., Li H., Brodkin E.S.: Genetic dissection of intermale aggressive behavior in BALB/cJ and A/J mice. Genes, Brain and Behavior 10: 57-68, 2011.

Fairless A.H., Dow H.C., Toledo M.M., Malkus K.A., Edelmann M., Li H., Talbot K., Arnold S.E., Abel T., Brodkin E.S.: Low sociability is associated with reduced size of the corpus callosum in the BALB/cJ inbred mouse strain. Brain Research 1230: 211-217, 2008.

Brodkin E.S.: Social behavior phenotypes in fragile X syndrome, autism, and the Fmr1 knockout mouse: Theoretical comment on McNaughton et al. (2008). Behavioral Neuroscience 122: 483-489, 2008.

Brodkin E.S.: BALB/cJ mice: low sociability and other phenotypes that may be relevant to autism. Behavioural Brain Research (Special Issue on “Animal Models for Autism”) 176: 53-65, 2007.

Sankoorikal G.M.V., Kaercher K.A., Boon C.J., Lee J.K., Brodkin E.S. : A mouse model system for genetic analysis of sociability: C57BL/6J vs. BALB/cJ inbred mouse strains. Biological Psychiatry 59: 415-423, 2006.

Gillihan S.J., Farah M.J., Sankoorikal G.M.V., Breland J., Brodkin E.S.: Association between serotonin transporter genotype and extraversion. Psychiatric Genetics 17: 351-354, 2007.

Brodkin E.S., Hagemann A., Nemetski S.M., Silver L.M. : Social approach-avoidance behavior of inbred mouse strains towards DBA/2 mice. Brain Research 1002: 151-157, 2004.

Brodkin E.S., Goforth S.A., Keene A.H., Fossella J.A., Silver L.M.: Identification of quantitative trait loci that affect aggressive behavior in mice. Journal of Neuroscience 22: 1165-1170, 2002.

Carlezon W.A., Thome J., Olson V.G., Lane-Ladd S.B., Brodkin E.S., Hiroi N., Duman R.S., Neve R.L., Nestler E.J.: Regulation of cocaine reward by CREB. Science 282: 2272-2275, 1998.

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Last updated: 09/16/2014
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