In the computational neuroscience Laboratory, we construct quantitative models of biological nervous systems that are firmly based on their neurophysiology, neuroanatomy and behavior, and that are developed in close interaction with experimentalists. Our main interest is neuronal function at the system level, reflecting the interaction of subsystems to generate useful behavior. Modeling is particularly important for understanding this and other system-level functions, since it requires the interaction of several pathways and neural functions. One of the functions we study is selective attention--that is, the capability of higher animals to scan sensory input for the most important information and to discard all other. Models of the neuronal basis of visual selective attention are constructed by simulating them on digital computers and comparing the results with data obtained from the visual and somatosensory systems of primates. We pay particular attention to the mechanisms involving the implementation of neural mechanisms that make use of the temporal structure of neuronal firing, rather than just the average firing rate.

The Bergles Laboratory studies synaptic physiology, with an emphasis on glutamate transporters and glial involvement in neuronal signaling. We are interested in understanding the mechanisms by which neurons and glial cells interact to support normal communication in the nervous system. The lab studies glutamate transport physiology and function. Because glutamate transporters play a critical role in glutamate homeostasis, understanding the transporters' function is relevant to numerous neurological ailments, including stroke, epilepsy, and neurodegenerative diseases like amyotrophic lateral sclerosis (ALS). Other research in the laboratory focuses on signaling between neurons and glial cells at synapses. Understanding how neurons and cells communicate, may lead to new approaches for stimulating re-myelination following injury or disease. Additional research in the lab examines how a unique form of glia-to-neuron signaling in the cochlea influences auditory system development, whether defects in cell communication lead to certain hereditary forms of hearing impairment, and if similar mechanisms are related to sound-induced tinnitus.

The Mollie Meffert Lab studies mechanisms underlying enduring changes in brain function. We are interested in understanding how programs of gene expression are coordinated and maintained to produce changes in synaptic, neuronal and cognitive function. Rather than concentrating on single genes, our research is particularly focused on understanding the upstream processes that allow neuronal stimuli to synchronously orchestrate both up and down-regulation of the many genes required to mediate changes in growth and excitation. This process of gene target specificity is implicit to the appropriate production of gene expression programs that control lasting alterations in brain function.

The research in the Svetlana Lutsenko Laboratory is focused on the molecular mechanisms that regulate copper concentration in normal and diseased human cells. Copper is essential for human cell homeostasis. It is required for embryonic development and neuronal function, and the disruption of copper transport in human cells results in severe multisystem disorders, such as Menkes disease and Wilson's disease. To understand the molecular mechanisms of copper homeostasis in normal and diseased human cells, we utilize a multidisciplinary approach involving biochemical and biophysical studies of molecules involved in copper transport, cell biological studies of copper signaling, and analysis of copper-induced pathologies using Wilson's disease gene knock-out mice.