Lynn T. Landmesser
Case Western Reserve University
|
Primary Section: 24, Cellular and Molecular Neuroscience Secondary Section: 28, Systems Neuroscience Membership Type:
Member
(elected 2001)
|
Biosketch
B.A. (1965) and Ph.D. (1969) degrees in Zoology from UCLA. Postdoctoral studies at the University of Utah School of Medicine (1969-1972). Faculty member in Biology at Yale University (1972-1983) rising from Assistant Professor to Professor with tenure, and beginning studies on the development of spinal cord motor circuits in avian and mouse embryos. Professor at the University of Connecticut, Department of Physiology and Neuroscience (1983-1993). Relocated to Case Western Reserve University Department of Neurosciences in 1993 and became the Arlene and Curtis Garvin Professor and Chair from 1997 until becoming Professor Emerita in 2014. Service on numerous editorial boards and government review panels, President of the Society for Developmental Biology (1988-89), Secretary of the Society for Neuroscience (1992-1994). Elected to the American Academy of Arts and Sciences (1993) and the National Academy of Sciences (2001). Also served on the HHMI Investigator Review Board (2001-2020) and the Advisory Board of the RIKEN Brain Science Institute in Japan (2003-2018).
Research Interests
The overall goal is to discover the cell and molecular mechanisms used by avian and mouse embryos to form the complex spinal motor circuits required for normal movement and locomotion. Processes studied include selective axon pathfinding, synapse formation and maturation, and the role of spontaneous, patterned electrical activity in these processes. Techniques include genetic and pharmacological/molecular manipulations, and electrical and optical recording and stimulation in ex-vivo spinal cords and in motoneuron-myotube cell cultures. Modest increases or decreases in the frequency of spontaneous bursting activity were recently shown to disrupt different aspects of motoneuron pathfinding, and underlying mechanisms are being investigated. A second research focus found that many aspects of mouse neuromuscular junction development and function were altered by deletion of specific isoforms of the neural cell adhesion molecule NCAM pre- or post-synaptically; these included targeting of exocytotic machinery to the synapse, a switch in Ca2+ channels, and an inability to cycle vesicles rapidly, resulting in transmission failures. Specific isoforms also were required in motoneuron-myotube cultures to transform motile growth cones into stable synapses. Alterations in synapse formation, maturation and stabilization contribute to many neurological disorders including spinal muscular atrophy.
