As a Postdoctoral Associate, the candidate will be working on an NIH-funded project investigating how cerebellar neurophysiology is disrupted by chronic glucose hypometabolism, the metabolic hallmark of GLUT1 deficiency syndrome (a genetic disorder producing ataxia). A second, complementary arm of the project examines a novel mutation in the DNA repair gene Rif1 that produces supernormal motor performance in mice, offering a contrasting model of enhanced cerebellar function. Using in vitro and in vivo preparations, the candidate will dissect cerebellar circuit-level changes using a combination of electrophysiological, pharmacological and imaging-based approaches.
The candidate will be responsible for the following:
Minimum Qualifications:
Preferred Qualifications:
Application Process:
Application entails curriculum vitae and three (3) letters of recommendation. Please submit these application documents to ChildNeuroJobs@med.cornell.edu
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