Tuesdays, Eccles (EIHG) Auditorium, 4:00-5:00 P.M.

September 16: Joe Fetcho, Ph.D., Cornell University

Department of Neurobiology and Behavior "Optical and genetic approaches toward understanding motor system function and dysfunction" Faculty host: Chi-Bin Chien, Neurobiology and Anatomy Student host: Renee Bend

Biosketch: The Fetcho lab uses zebrafish to study how motor neurons of the brain and spinal cord produce movements. They use genetic manipulations and lesions combined with high-speed imaging to determine the contributions of individual neurons to escape behaviors. Further, using cell labeling and physiological methods, they are uncovering the neural circuitry and molecular events underlying escape behaviors. They are also interested in spinal cord regeneration. In zebrafish, spinal motor neurons do not normally regenerate after injury, however the Fetcho lab is exploring manipulations that allow regeneration to occur. Following these manipulations they can live-image axon regeneration in real time due to the transparency of zebrafish larvae.

October 21: Scott Baraban, Ph.D., University of California, San Francisco

Department of Neurological Surgery "Epilepsy Investigations and Potential Pathways to a Cure" Faculty host: Steve White, Pharmacology & Toxicology Student host: Eli Iacob

Biosketch: Scott C. Baraban is the William K. Bowes Jr. Endowed Chair in Neuroscience Research and Director of the Epilepsy Research Laboratory at UCSF. He received a PhD in Pharmacology from the University of Virginia and completed post-doctoral training with Drs. Philip Schwartzkroin and Richard Palmiter at the University of Washington. Research in the Baraban laboratory focuses on the neurobiological basis of epilepsy and in developing novel treatments. He is currently investigating strategies to generate new inhibitory neurons from neural progenitor cells and using these to treat mouse models of epilepsy. His group also focuses on malformations of cortical development and the changes in circuitry that can lead to seizures in these types of conditions. This work is largely performed in rodents, but the lab has also established novel seizure models in zebrafish and recently completed a large-scale mutagenesis screen to identify seizure resistant mutants.

November 18: Maureen Neitz, Ph.D., Medical College of Wisconsin

Department of Cell Biology, Neurobiology and Anatomy "Gene therapy cure for color blindness in an adult primate" Faculty host: Robert Marc, Ophthalmology and Visual Sciences Student host: James Tucker

Biosketch: Maureen and her husband Jay Neitz study how photoreceptors select the spectral visual pigments they express and how the organization of the primate pigments determines visual performance. The Neitzes have recently worked out the molecular mechanisms underlying the huge diversity of color processing diversity in normal and aberrant human color vision and why that differs from other primates. In a recent groundbreaking experiment, they demonstrated that dichromatic primates can be made trichromatic by in-vivo viral delivery of visual pigments to the photoreceptors. A long-term goal of the laboratory is to extend our basic knowledge of the role that genes play in the construction of the nervous system.

December 16: Gregg Recanzone, Ph.D., University of California, Davis

Biosketch: Research in the Recanzone lab involves investigating the role of the cerebral cortex in the perception of auditory signals. Lesions of the auditory cortex in humans and animals result in two main deficits: the ability to determine the location of sounds and the ability to process sounds that vary rapidly in time, such as most environmental noises and human speech. While the cerebral cortex is obviously important for these fundamental perceptions, the neuronal mechanisms that underlie these perceptions are poorly understood. The main focus of the lab has been in the processing of sound location, and most recently in defining the interactions between auditory and visual stimuli in the perception of the location of combined auditory and visual stimuli. Under normal conditions, visual stimuli "capture" the perceived location of auditory stimuli, generating the ventriloquism illusion. Under the appropriate circumstances, this illusion can be long-lasting, a phenomenon known as the ventriloquism aftereffect. The presence of this aftereffect indicates that the spatial representation of multi-sensory stimuli must be plastic and can be altered in the adult within minutes to tens of minutes.

January 20: Dwight Bergles, Ph.D., Johns Hopkins University School of Medicine

Solomon H. Snyder Department of Neuroscience "Sounds in silence: How the ear generates noise during development" Faculty host: Karen Wilcox, Pharmacology and Toxicology Student host: Koji Takahashi

Biosketch: The Bergles laboratory is interested in understanding the mechanisms by which neurons and glia interact to support normal communication in the nervous system. The glial specific glutamate transporters are responsible for the uptake of extracellular glutamate at excitatory synapses. Thus, they shape the tone of synaptic activation and prevent excitotoxicity by limiting the availability of free glutamate. By studying glial glutamate transport currents, electrophysiological studies in the Bergles lab is revealing the properties of glutamate release and diffusion, transporter kinetics, and the roles they play in development and disease. In addition, the lab has also discovered glutamatergic synapses between pyramidal cells and NG2+ oligodendrocyte precursor cells. By studying this unique neuron-glia communication, they hope to determine its role in normal hippocampal physiology and myelination. Finally, the lab also studies glial physiology in the cochlea. A population of astrocyte-like support cells surrounds the inner hair cells (IHCs), the sensory receptor cells in the cochlea. These support cells express the glutamate-aspartate transporter GLAST and are responsible for clearing glutamate at the IHC-auditory afferent synapse. They are interested in further elucidating their role in shaping synaptic transmission in response to sound. The lab has also found that these supporting cells are electrically active during cochlear development and determined that they initiate electrical activity in auditory nerves before the onset of hearing. They are currently investigating how this unique form of glia to neuron signaling influences auditory system development, whether defects in supporting cell to IHC communication underlie hereditary forms of hearing impairment, and if similar mechanisms are implicated in the initial stages of sound-induced tinnitus.

February 17: Michael Ehlers, M.D., Ph.D., Duke University Medical Center

Department of Neurobiology, Howard Hughes Medical Institute "Memory and Membrane Dynamics in Dendritic Microcompartments" Faculty host: Villu Maricq, Biology Student host: Eerik Elias

Biosketch: Michael Ehlers is interested in the mechanisms and organelles underlying protein trafficking and turnover in neuronal dendrites and their relation to neural circuit plasticity. He has demonstrated different methods neurons use to self-regulate electrical activity, adjusting the level of protein receptors in the postsynaptic membrane to strengthen connections with neighboring neurons (a key feature of learning and memory) or dampen them, allowing the neuron to "reset." He showed recently that cell structures called recycling endosomes trigger a prolonged burst in a neuron's electrical activity by causing a surge in so-called AMPA receptors. He also demonstrated that neurons increase their sensitivity by "alternate splicing" of NMDA receptors to generate extra variants. Ehlers plans to use biochemical, optical imaging, and biophysical approaches to probe the internal organization of neurons, including the nanoarchitecture of brain synapses, to reveal fundamental mechanics of brain cell communication.

March 17: Ferdinando Mussa-Ivaldi, Ph.D., Northwestern University

Departments of Physiology, Physical Medicine Rehabilitation, and Mechanical Engineering "The representation of space and time through sensory-motor learning" Faculty host: Bradley Greger, Bioengineering Student host: Rebecca Parker

Biosketch: Dr. Ferdinando (Sandro) Mussa-Ivaldi is the founder and director of the Robotics Lab at the Rehabilitation Institute of Chicago, and a professor at Northwestern University. He received a Bachelors degree in physics from the University of Torino, and a PhD in biomedical engineering from the PolyTechnic University of Milan. His research uses both experimental and theoretical approaches to study how coordinated movements are learned and executed. Dr. Mussa-Ivaldi did a remarkable study that bidirectionally connected tissue from a lamprey brain with a robot that was actually able to move! Converting brain output to motor output is critical to the development of prostheses.

April 21: Marie Filbin, Ph.D., Hunter College, CUNY

Department of Biology "Signaling Regeneration in the Adult CNS" Faculty host: Shannon Odelberg, Internal Medicine Student host: Katherine Zukor

Biosketch: Dr. Marie Filbin is a Distinguished Professor and Director of the Specialized Neuroscience Research Program at Hunter College, City University of New York in Manhattan. She received BS and PhD degrees from the University of Bath, UK and completed a post-doctoral fellowship at Johns Hopkins Medical School. Research in Dr. Filbin's laboratory focuses on the roles that myelin and myelin-associated glycoprotein (MAG) have in preventing axon regeneration after spinal cord injury in adult mammals. While MAG had been shown to promote neurite outgrowth from embryonic neurons, her research team discovered that MAG inhibits outgrowth from adult neurons and that a neuron's intracellular level of cAMP determines how it responds to MAG. Her lab is continuing to unravel the molecular details of MAG's complex effects on axon regeneration and is devising ways to block MAG's inhibitory effects or alter a neuron's intracellular levels of cAMP to change how the neuron responds to MAG. Knowledge gained from Dr. Filbin's research has real potential to improve treatments for humans with spinal cord injury.

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