The Paul Worley Lab examines the molecular basis of learning and memory. In particular, we cloned a set of immediate early genes (IEGs) that are rapidly transcribed in neurons involved in information processing, and that are essential for long term memory. IEG proteins can directly modify synapses and provide insight into cellular mechanisms that support synapse-specific plasticity.

The Christopher Potter Lab functions at an intersection between systems and cellular neuroscience. We are interested in how neurons and circuits function in the brain to achieve a common goal (olfaction), but we also develop, utilize and build tools (molecular and genetic) that allow us to directly alter neuronal functions in a living organism. The specific focus of my laboratory is to understand how the insect brain receives, interprets, and responds to odors. Insects rely on their sense of smell for all major life choices, from foraging to mating, from choosing where to lay eggs to avoiding predators and dangers. We are interested in understanding at the neuronal level how odors regulate these behaviors. Our long-term aim is to apply this knowledge to better control insects that pose a threat to human health. Our general approach towards achieving this goal is to develop and employ new genetic methods that enable unprecedented control over neural circuits in both the model organism Drosophila melanogaster and human malaria vector Anopheles gambiae.

The Kristina Nielsen Laboratory investigates neural circuits in the visual cortex that are responsible for encoding objects to understand how the visual system performs object recognition. We aim to reveal the fine-scale organization of neural circuits, with an emphasis on higher-level visual areas. We use two-photon microscopy to perform high-resolution functional imaging of visual areas in the non-human primate. We also investigate how the function of higher visual areas changes over the course of brain development in ferrets, by measuring the activity of single neurons in these areas, as well as determining the animal's visual capabilities at various developmental stages. In both types of investigations, we also rely on detailed anatomical techniques to precisely observe how the function of neuronal circuits is related to their structure.

The Fuchs Laboratory uses cellular electrophysiology, immunolabeling and electron microscopy to study synaptic connections between sensory hair cells and neurons in the cochlea. One effort focuses on an unusual cholinergic receptor that mediates efferent inhibition of hair cells, driving discovery of the molecular mechanisms, and offering a target for protection against acoustic trauma. A second topic concerns the small number of unmyelinated ""type II"" afferent neurons whose synaptic connectivity and response properties argue for a role as the pathway for noxious (too loud) sound. Our studies are motivated by curiosity about fundamental mechanisms, and to provide a foundation for understanding cochlear pathogenesis.

The Shanthini Sockanathan Laboratory uses the developing spinal cord as our major paradigm to define the mechanisms that maintain an undifferentiated progenitor state and the molecular pathways that trigger their differentiation into neurons and glia. The major focus of the lab is the study of a new family of six-transmembrane proteins (6-TM GDEs) that play key roles in regulating neuronal and glial differentiation in the spinal cord. We recently discovered that the 6-TM GDEs release GPI-anchored proteins from the cell surface through cleavage of the GPI-anchor. This discovery identifies 6-TM GDEs as the first vertebrate membrane bound GPI-cleaving enzymes that work at the cell surface to regulate GPI-anchored protein function. Current work in the lab involves defining how the 6-TM GDEs regulate cellular signaling events that control neuronal and glial differentiation and function, with a major focus on how GDE dysfunction relates to the onset and progression of disease. To solve these questions, we use an integrated approach that includes in vivo models, imaging, molecular biology, biochemistry, developmental biology, genetics and behavior.

Research in the Raymond Koehler Lab explores cerebrovascular physiology and cerebral ischemic injury caused by stroke and cardiac arrest, using protein analysis, immunohistochemistry and histology. We also study ischemic preconditioning, neonatal hypoxic-ischemic encephalopathy and the mechanisms of abnormal cerebrovascular reactivity after ischemia. We 're examining ways to improve tissue oxygenation and seek to better understand the mechanisms that connect an increase in cerebral blood flow to neuronal activity.

Researchers in the Adam Sapirstein Lab focus on the roles played by phospholipases A2 and their lipid metabolites in brain injury. Using in vivo and in vitro models of stroke and excitotoxicity, the team is examining the roles of the cytosolic, Group V, and Group X PLA2s as well as the function of PLA2s in cerebrovascular regulation. Investigators have discovered that cPLA2 is necessary for the early electrophysiologic changes that happen in hippocampal CA1 neurons after exposure to N-methyl-d-aspartate (NMDA). This finding has critical ramifications in terms of the possible uses of selective cPLA2 inhibitors after acute neurologic injuries.

Research in the James Knierim Laboratory attempts to understand the flow of information through the hippocampal formation and the computations performed by the various subfields of the hippocampus and its inputs from the entorhinal cortex. To address these issues, we use multi-electrode arrays to record the extracellular action potentials from scores of well-isolated hippocampal neurons in freely moving rats. These neurons, or ""place cells,"" are selectively active when the rat occupies restricted locations in its environment and help to form a cognitive map of the environment. The animal uses this map to navigate efficiently in its environment and to learn and remember important locations. These cells are thought to play a major role in the formation of episodic (autobiographical) memories. Place cells thus constitute a tremendous opportunity to investigate the mechanisms by which the brain transforms sensory input into an internal, cognitive representation of the world and then uses this representation as the framework that organizes and stores memories of past events.

Researchers in the C. David Mintz Lab seek to better understand the specific methods by which anesthesia can impair a patient’s brain development. Recent studies have investigated the ways in which anesthetics interfere with axon guidance in developing mouse neocortical neurons via a GABAA receptor mechanism, as well as the method by which anesthetics interfere with the polarization of developing cortical neurons.

The Cochlear Neurotransmission Group studies the generation and propagation of neural signals in the inner ear. Our laboratories use biophysical, electrophysiological, molecular biological and histological methods to determine fundamental molecular mechanisms by which neurotransmitters are released from primary sensory cells ('hair cells') to excite second order neurons carrying information to the brain. We apply these same techniques to study inhibitory feedback produced by brain neurons that project to and regulate the sensitivity of the cochlea.