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 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.

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 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.

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.

Human induced pluripotent stem cells (hiPSCs) provide unprecedented opportunities for cell replacement approaches, disease modeling and drug discovery in a patient-specific manner. The Gabsang Lee Lab focuses on the neural crest lineage and skeletal muscle tissue, in terms of their fate-determination processes as well as relevant genetic disorders. Previously, we studied a human genetic disorder (familial dysautonomia, or FD) with hiPSCs and found that FD-specific neural crest cells have low levels of genes needed to make autonomous neurons--the ones needed for the ""fight-or-flight"" response. In an effort to discover novel drugs, we performed high-throughput screening with a compound library using FD patient-derived neural crest cells. We recently established a direct conversion methodology, turning patient fibroblasts into ""induced neural crest (iNC)"" that also exhibit disease-related phenotypes, just as the FD-hiPSC-derived neural crest. We're extending our research to the neural crest's neighboring cells, somite. Using multiple genetic reporter systems, we identified sufficient cues for directing hiPSCs into somite stage, followed by skeletal muscle lineages. This novel approach can straightforwardly apply to muscular dystrophies, resulting in expandable myoblasts in a patient-specific manner.

Research in the Glowatzki Lab focuses on the auditory system, with a particular focus on synaptic transmission in the inner ear. Our lab is using dendritic patch clamp recordings to examine mechanisms of synaptic transmission at this first, critical synapse in the auditory pathway. With this technique, we can diagnose the molecular mechanisms of transmitter release at uniquely high resolution (this is the sole input to each afferent neuron), and relate them directly to the rich knowledge base of auditory signaling by single afferent neurons. We study pre- and post-synaptic mechanisms that determine auditory nerve fiber properties. This approach will help to study general principles of synaptic transmission and specifically to identify the molecular substrates for inherited auditory neuropathies and other cochlear dysfunctions.

The Brown Lab is focused on the function of the cerebral cortex in the brain, which underlies our ability to interact with our environment through sensory perception and voluntary movement. Our research takes a bottom-up approach to understanding how the circuits of this massively interconnected network of neurons are functionally organized, and how dysfunction in these circuits contributes to neurodegenerative diseases like amyotrophic lateral sclerosis and neuropsychiatric disorders, including autism and schizophrenia. By combining electrophysiological and optogenetic approaches with anatomical and genetic techniques for identifying cell populations and pathways, the Brown Lab is defining the synaptic interactions among different classes of cortical neurons and determining how long-range and local inputs are integrated within cortical circuits. In amyotrophic lateral sclerosis, corticospinal and spinal motor neurons progressively degenerate. The Brown Lab is examining how abnormal activity within cortical circuits contributes to the selective degeneration of corticospinal motor neurons in an effort to identify new mechanisms for treating this disease. Abnormalities in the organization of cortical circuits and synapses have been identified in genetic and anatomical studies of neuropsychiatric disease. We are interested in the impact these abnormalities have on cortical processing and their contribution to the disordered cognition typical of autism and schizophrenia.

The Dong Laboratory has identified many genes specifically expressed in primary sensory neurons in dorsal root ganglia (DRG). Our lab uses multiple approaches, including molecular biology, mouse genetics, mouse behavior and electrophysiology, to study the function of these genes in pain and itch sensation. Other research in the lab examines the molecular mechanism of how skin mast cells sensitize sensory nerves under inflammatory states.

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.