eagle-i University of PennsylvaniaUniversity of Pennsylvania
See it in Search

Brodkin Laboratory


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.




Organisms and Viruses

  • B6.129P2-Fmr1tm1Cgr/J ( Mus musculus )

    "These Fmr1 knockout mice have a neomycin resistance cassette replacing exon 5 of the fragile X mental retardation syndrome 1 (Fmr1) gene. Defects in FMR1 cause Fragile X syndrome, one of the most common forms of inherited mental retardation. Fragile X syndrome is associated with an array of deficits in motor control, cognition, learning, and memory, although their overall brain morphology is generally normal. Male hemizygotes and female homozygotes are viable and fertile. Male hemizygotes show macroorchidism (enlarged testes). Macroorchidism in caused by an increased rate of Sertoli cell proliferation during embryogenesis which may be independent of FSH signalling. Male hemizygotes and females homozygotes also exhibit hyperactivity, learning deficits, altered dendritic spines of visual cortex pyramidal cells, and differences in a variety of behavioral tests. Comparison of homozygotes to wildtype littermates in hidden- and visible-platform water maze learning showed deficits in spatial learning and motor performance."

Web Links:

Last updated: 2019-11-21T14:51:53.025-05:00

Copyright © 2016 by the President and Fellows of Harvard College
The eagle-i Consortium is supported by NIH Grant #5U24RR029825-02 / Copyright 2016