Rita Cowell, Ph.D.

rcowellAssistant Professor

Primary Department Affiliation
: Psychiatry and Behavioral Neurobiology
Primary Research Area: Learning, Memory, and Synaptic Plasticity
Neurodevelopment and Developmental Disabilities

Email: rcowell@uab.edu
Phone: 205.975.7466

Recent Publications


  • BS Biology, University of Illinois, Champaign-Urbana, 1997; PhD Neuroscience, University of Michigan, 2002; Postdoctoral Fellow, University of Michigan 2002-2006.

Academic Appointments with UAB:

  • Assistant Professor of Psychiatry and Behavioral Neurobiology, Cell Biology, and Neurobiology
  • Secondary Appointment in Psychology
  • Associate Scientist, Civitan International Research Center

People in the Lab:

  • J. Doug Morgan - Research Assistant, jdmorgan@uab.edu
  • Elizabeth Lucas - Third year Graduate Student, Dept. Psychology, befluvsu@uab.edu
  • J. Matt Rutherford - Third year MSTP Student, Dept. Neurobiology, ruther@uab.edu
  • Pratik Talati - Undergraduate Research Assistant, pratik@uab.edu
  • Alec Lewis - Undergraduate Research Assistant, ablewis@uab.edu
  • Courtney Sparkman - Undergraduate Research Assistant, cspark@uab.edu

  • Transcriptional Regulation of Early Postnatal Brain Development: Insights into the Pathology of Autism and Schizophrenia
  • Recent developments have lead to the understanding that autism and schizophrenia are neurodevelopmental disorders influenced by both environmental and genetic factors. One way in which environmental stimuli can influence gene transcription is by altering chromatin structure (methylation/acetylation) and the formation of transcriptional complexes. Our laboratory determined that the transcriptional coactivator PGC-1a, a protein involved in the control of metabolic gene expression in non-neuronal tissues, is concentrated in inhibitory interneurons during early postnatal rat brain development. Interestingly, inhibitory interneurons are dysfunctional in a variety of disorders, including autism, schizophrenia and epilepsy. Our laboratory is currently using Western blotting, RT-PCR, immunocytochemistry/confocal microscopy, chromatin immunoprecipitation assays, and targeted gene knockout technologies in cell culture and rodents to investigate the roles of PGC-1a and chromatin modifications in normal and pathological brain development. In addition, we are using single-cell laser capture to isolate neurons from post-mortem human brain tissue to determine whether there are cell-specific changes in gene expression in schizophrenia. These studies are aimed at elucidating how perturbations in gene expression during development contribute to the progression of neurodevelopmental disorders.

Recent Publications:

Cowell RM
, Blake KR, Russell JW. (2007) Localization of the transcriptional coactivator PGC-1α to GABAergic neurons during maturation of the rat brain. J. Comp. Neurol. 502:1-18.

Cowell RM
, Xu H, Parent JM, Silverstein FS. (2006) Microglial expression of chemokine receptor CCR5 during rat forebrain development and after perinatal hypoxia-ischemia. J. Neuroimmunol. 173:155-65.

Cowell RM
, Silverstein FS. (2003) Developmental changes in the expression of chemokine receptor CCR1 in the rat cerebellum. J. Comp. Neurol. 457:7-23.

Cowell RM
, Plane JM, Silverstein FS. (2003) Complement activation contributes to hypoxic-ischemic brain injury in neonatal rats. J. Neurosci. 23:9459-68.

Cowell RM
, Xu H, Galasso JM, Silverstein FS. (2002) Hypoxic-ischemic injury induces macrophage inflammatory protein-1a expression in immature rat brain. Stroke. 33:795-801.