April 20, 2001

Colloquium Speaker: Kenna Peusner


Professor Kenna D. Peusner received her B.S. degree in biology from Simmons College and her Ph.D. in anatomy from Harvard University. In 1975, she joined the Jefferson Medical College where she received the first (1979) of 6 NIH grants as Principal Investigator and the Lindback Foundation Award for distinguished teaching in the basic medical sciences (1981). Since 1981, she has been at George Washington University Medical Center where she is currently Professor of Anatomy and Cell Biology. In 1986, she spent a sabbatical year at the Pasteur Institute, Paris. Professor Peusner, long known for studying the morphological development of the vestibular system at the cellular level, has since 1986, included developmental physiology in her research by introducing electrophysiological investigations on brain slices. This combined structure-function approach used to study identified neurons, has resulted in the routine performance of state-of-the-art intracellular and patch-clamp recordings in her laboratory which is the only one in the US focused on investigating the development of vestibular nuclei neurons. Dr. Peusner is a member of the Neuroscience Society, Association for Research in Otolaryngology, AAAS and is a former member of the Committee for Space Biology and Medicine, NRC/NAS (1995-2000).


Colloquium Topic: A Promising Model to Investigate Brain Plasticity

Neuroplasticity refers to the long-lived alterations in structure and function that neurons may undergo after changes in their activity. The degree of alteration depends in part on the type of lesion or change, on the age of the animal and the time during development of the system when the change occurs. Such alterations range from gross to microscopic and molecular, involving cell death, cell atrophy, loss of dendrites, synaptic reorganization, and long term potentiation (LTP), depression, or changes in efficacy of synaptic transmission. The types of changes in stimuli that may lead to neuroplasticity are diverse, including eyelid closure in the visual system, cochlear deprivation or overstimulation in the auditory system, labyrinthectomy in the vestibular system, whisker removal in the somatosensory system, or simple nerve transection of any afferent input or change in frequency of firing of the afferent fibers. Neuroplasticity results in changes in the function of not only a single target neuron, but may also lead to changes in the function of the entire pathway or system in which the target neuron participates. Accordingly, the effects on the organism can be profound. Neuroplasticity can result in enhanced performance. There is an important type of plasticity that is exhibited by the vestibular system in response to labryrinthectomy, vestibular nerve transaction or exposure to microgravity. This is commonly called vestibular compensation. After the lesion or on exposure to microgravity, multiple symptoms are observed which diminish or disappear after about a week in most adult mammals. Presently, the mechanisms underlying vestibular compensation are thought to be mediated by modifications in synapses, most likely those within the vestibular nuclei, although other brainstem neurons and parts of the cerebellum have been implicated. Our working hypothesis is that vestibular neurons recover function after a peripheral vestibular lesion by repeating certain aspects of their normal development.