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The laboratory of Dr. Valeria Cavalli is seeking passionate scientists to join their team and contribute to our NIH-funded research projects on the multicellular mechanisms promoting axon regeneration in mouse and human models.

PI: Linda Richards AO, FAA, FAHMS, PhD, department chair

The Richards Lab focuses on the development, plasticity and function of long-range connections of the cerebral cortex. The corpus callosum is the largest fibre tract in the brain of placental mammals and connects neurons in each cortical hemisphere. The lab investigates how cellular and molecular/genetic mechanisms regulate brain wiring during development and how brain wiring is altered in congenital corpus callosum dysgenesis (CCD).

PI: Terry Ritzman, PhD

The Ritzman Lab is interested in the comparative anatomy of the skull in primates as it relates to human evolution. The lab employs the comparative method and direct studies of fossil hominins to make inferences regarding the evolutionary processes that operated during the course of human evolution, as well as the patterns, documented by the fossil record, that were produced by these processes.

The Robert J. Terry lecture acknowledges the contributions of Dr. Terry to the teaching on human anatomy. He was a leader in the anatomy department at WashU Medicine for more than four decades.

PI: Lawrence Salkoff, PhD

The Salkoff Lab studies potassium channels which are key elements which control and shape electrical activity in the brain, heart, and other excitable tissues. These channels are major determinants of behavior and higher brain function.

Avraham, O., Deng, P. Y., Jones, S., Kuruvilla, R., Semenkovich, C. F., Klyachko, V. A. & Cavalli, V., Dec 1 2020, In: Nature communications. 11, 1, 4891.

PI: Paul Shaw, PhD

The Shaw Lab uses the genetic model organism Drosophila melanogaster to elucidate the molecular mechanisms linking sleep to neuronal plasticity. The lab has demonstrated that we can fully restore cognitive functioning to a diverse set of classic memory mutants simply by enhancing their sleep. In these experiments, sleep was able to reverse cognitive deficits without restoring the causal molecular lesion or structural defect. In addition sleep reversed cognitive deficits in two separate models of Alzheimer’s disease.