Education
- BS in Neurobiology, Physiology, and Behavior, University of California Davis, Davis, CA
- PhD in Neuroscience, Vollum Institute, Oregon Health and Sciences University, Portland, OR (Laboratory of John. T. Williams)
- Postdoctoral Fellow, Department of Anesthesiology, Oregon Health and Sciences University, Portland, OR (Laboratory of Paco S. Herson)
- Postdoctoral Fellow, Department of Anesthesiology, University of Colorado School of Medicine, Aurora, CO (Laboratory of Paco S. Herson)
Contact Information
Mail Stop 8130
12801 E. 17th Avenue, Rm L18-4105
Aurora, CO 80045
Telephone: (303) 724-6629
Email: nidia.quillinan@cuanschutz.edu
Training Programs
Research Interests
The Quillinan laboratory studies excitability and plasticity changes in the brain following cerebral ischemia. We are particularly interested in cerebellar networks that are affected by stroke and cardiac arrest. We also investigate the role of sex hormones and their receptors in acute neuronal injury and longterm hippocampal function.
Research Description
We are pre-clinical basic science lab that investigates excitability and plasticity changes that contribute to neurological deficits. Our overarching goal is to identify therapeutic strategies to improve neuronal network function that will improve neurological outcome after brain injury. We use a multidisciplinary approach that includes in vivo animal models, electrophysiology, molecular analysis of gene and protein expression and virus-mediated gene manipulation. Current projects in the lab are aimed at investigating motor and cognitive deficits after cerebellar ischemia and changes in functional connectivity of the cerebellum with forebrain areas. We are examining thalamic excitability and hippocampal synaptic function after cerebellar stroke using slice electrophysiology. We also study sex- and age-dependent mechanisms that contribute to neuronal injury and plasticity deficits in the hippocampus. We are particularly interested in how sex hormones contribute to injury and repair throughout the lifespan. Experiments utilize hormone manipulations, histological and morphological analysis of hippocampal neurons and viral-mediated gene silencing to interrogate the contribution of sex steroid receptors to cardiac arrest-induced memory deficits.