Laurel Carney, Ph.D.
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- Auditory Neuroscience
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We combine neurophysiological, behavioral, and computational modeling techniques towards our goal of understanding neural mechanisms underlying the perception of complex sounds. Most of our work is focused on hearing in listeners with normal hearing ability. We are also interested in applying the results from our laboratory to the design of physiologically based signal-processing strategies to aid listeners with hearing loss.\nWe are currently studying two specific problems: detection of acoustic signals in background noise, and detection of fluctuations in the amplitude of sounds. These problems are of interest because they are tasks at which the healthy auditory system excels, but they are situations that can present great difficulty for listeners with hearing loss. We study the psychophysical limits of ability in these tasks, and we also study the neural coding and processing of these sounds using stimuli matched to those of our behavioral studies. Computational modeling helps bridge the gap between our behavioral and physiological studies. For example, using computational models derived from neural population recordings, we make predictions of behavioral abilities that can be directly compared to actual behavioral results. The cues and mechanisms used by our computational models can be manipulated to test different hypotheses for neural coding and processing.\nBy identifying the cues involved in the detection of signals in noise and fluctuations of signals, our goal is to direct novel strategies for signal processors to preserve, restore, or enhance these cues for listeners with hearing loss. Read more
For specific questions, please contact me via email.
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Deborah Cory-Slechta, Ph.D.
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- Environmental neurotoxicants as risk factors for neurodevelopmental and neurodegenerative diseases and disorders
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This laboratory focuses on understanding the role of environmental chemical exposures as etiologic factors for neurodevelopmental and neurodegenerative diseases and disorders. These studies encompass both experimental animal and human translational efforts. One focus area explores the contribution of pesticide exposures to the etiology of the Parkinson’s disease phenotype. Our laboratory has developed both young adult and developmental pesticide exposure models of the phenotype, has determined how age, gender, and genetic background alter the influence of pesticides in these models, and begun to explore how oxidative stress and inflammatory mechanisms contribute to the dopamine neurodegeneration. Future studies aim to determine biochemical mechanisms and markers that are common across models of the Parkinson’s disease phenotype as points of dopamine system vulnerability. Read more
For specific questions, please contact me via email.
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Kevin A. Davis, Ph.D.
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- Auditory Neurophysiology
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To study the organization and function of the anatomical pathways in the brain that are responsible for localizing sounds in space. Read more
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Greg DeAngelis, Ph.D.
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- Neural mechanisms of depth perception
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The image formed on each retina is a two-dimensional projection of the three-dimensional (3D) world. Objects at different depths project onto slightly disparate points on the two retinas, and the brain is able to extract these binocular disparities from the retinal images and construct a vivid sensation of depth. My lab studies the mechanisms by which binocular disparity information is encoded, processed, and read out by the brain in order to perceive depth and compute 3D surface structure. We have also recently discovered a population of neurons that combines visual motion with eye movement signals to code depth from motion parallax, thus constituting a new neural mechanism for coding depth. Future work will focus on how depth cues from disparity and motion parallax are integrated by neurons. Read more
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- Sensory integration for self-motion perception.
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To accurately perceive our own motion through space, we integrate information from the visual and vestibular systems. Because visual and vestibular signals originate in different spatial frames of reference and with different temporal dynamics, an interesting set of computations must occur in order for these cues to be combined perceptually. Using a 3D virtual reality system to provide monkeys with naturalistic combinations of visual stimuli and inertial motion, we are studying how cortical neurons integrate visual and vestibular signals to compute one's direction of heading through 3D space. Read more
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Edward G. Freedman, Ph.D.
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- Neural Control of Coordinated Movements
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My research focuses on understanding the neural computations involved in the coordination of visual orienting movements. We use neurophysiological techniques, computer modeling, and analysis of behavior in order to test specific predictions of our hypotheses. Current projects include the role of brainstem neurons in eye-head coordination, role of cerebellar Purkinje cells in motor learning processes, human eye-head coordination, and the potential role of adaptive filters in the oculomotor system. A rotation in the lab would expose graduate students to the use and care of non-human primates, neurophysiological techniques, analysis of human and non-human behavioral data and use of computer models to generate testable predictions. Read more
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Lin Gan, Ph.D.
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- Transcription factors in neurogenesis
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My research focuses on identifying transcription factors and regulatory pathways required for neuronal cell differentiation in various nervous systems including the mammalian retina, inner ear, spinal cord, and neocortex. We are currently investigating the regulatory pathways comprised of three major classes of transcription factors: the basic helix-loop-helix (bHLH), the LIM-domain, and the Class IV POU-homeodomain transcription factors. Using genetically modified mice (transgenic and knockout mice), we have shown that these three classes of transcription factors function in transcription factor cascades to regulate the patterning and cell fate specification during neurodevelopment. Read more
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Dana Helmreich, Ph.D.
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- Neuroendocrine consequences of two animal models of active behavioral coping.
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The overall goal of the experiments is to examine neuroendocrine systems during stress, and more importantly, during models of active behavioral coping. Successful coping with stress is necessary to promote individual resiliency and to prevent pathological outcomes, such as depression, associated with prolonged stress exposure. Neuroendocrine systems are important systems to study as the end products (hormones) have receptors throughout the body including the central nervous system, and the genomic actions of the receptors can produce long lasting changes in both physiology and behavior. The stress/coping paradigms will be examined in adult male rats. Read more
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Krystel R. Huxlin, Ph.D.
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- Visual perceptual plasticity in adulthood - properties and mechanisms
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In mammals, most visual information destined for conscious perception is sent from the eyes, through the dorsal lateral geniculate nucleus of the thalamus to primary visual cortex. From there, the information is distributed to and processed by several, extra-striate visual cortical areas. Since it acts as a major gateway to the rest of the visual cortical system, V1 damage causes profound, homonymous losses in visual perception, referred to as "cortical blindness". Traditionally, cortical blindness has been considered recalcitrant to rehabilitation and permanently disruptive to almost every aspect of daily life, affecting mobility, depth perception, reading and driving. This contrasts with the known ability of visual systems to learn, improve in sensitivity, and remember. Why can't such clear potential for plasticity be used to induce recovery of visual perception after visual cortical damage? Our laboratory employs psychophysical studies, experiments involving virtual and naturalistic vision, as well as functional imaging (magnetic resonance imaging) to answer this question and study the limits for visual plasticity in the adult brain. We are particularly interested in: (1) identifying means of increasing or decreasing visual plasticity, (2) characterizing differences in plastic potential between intact and damaged, adult visual systems, (3) assessing differences between visual plasticity in complex, naturalistic environments, and the more simplified visual environments typical of most laboratory and clinical testing conditions, and (4) understanding how visual training induces visual plasticity. In addition to significantly increasing our understanding of sensory plasticity in adulthood, this work has serious implications for the design and implementation of therapeutic strategies for those suffering from visual deficits. Read more
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Paul J. Kammermeier, Ph.D.
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- metabotropic glutamate receptor signaling in neurons
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We use patch-clamp electrophysiology and molecular biological tools to study metabotropic glutamate receptor signaling in neurons. We are primarily focused on three areas of research: 1) The role of Homer proteins in regulating the function of mGluR1 and 5; 2) Signaling of mGluR6, a specialized receptor expressed at high levels only in a specific type of retinal neuron; and 3) The role of dimerization in mGluR signaling. Read more
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- Modulation of native calcium and potassium currents by heterologously expressed mGluRs in rat sympathetic neurons
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We use electrophysiological techniques to examine the modulation of native calcium and potassium currents by heterologously expressed mGluRs in rat sympathetic neurons, and the regulation of synaptic currents by native mGluRs in hippocampal neurons. We are also beginning to examine mGluR6 signaling in retinal ON bipolar cells from the rat and from specific mouse models. Read more
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- Mechanism of metabotropic glutamate receptor signaling and ion channel modulation in neurons.
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We are interested in the signaling mechanisms of the mGluR class of G protein coupled receptors, the physiological role of their modulation of voltage dependent ion channels and synaptic currents, and the proteins that regulate these processes in central and peripheral neurons. Read more
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Ania K. Majewska, Ph.D.
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- Mechanisms of Plasticity in the Visual System
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During a late developmental period closure of one eye (monocular deprivation) results in plasticity of visual cortical neurons such that responses to visual stimulation of the closed eye are diminished. We have recently characterized structural changes at synapses that occur during monocular deprivation and are currently studying the mechanisms of synaptic structural and functional plasticity. A rotation in the lab would expose students to rodent surgeries, in vivo and in vitro imaging, electrophysiology and immunocytochemistry. Read more
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Margot Mayer-Pröschel, Ph.D.
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- Cellular and molecular targets of embryonic iron deficiency
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We recently identified two novel molecular targets that seem to be disrupted during iron deficiency. The deregulation of these targets leads to increase proliferation in glial precursor cell populations and seems to be involved in a fate in the glial lineage switch during embryogenesis. The candidate will be involved in the further characterization of these targets by performing in-situ hybridizations, anti-sense RNA targeting and primary cell tissue culture experiments. Read more
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John A. Olschowka, Ph.D.
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- Role of the cytokine HMGB1 and its receptor in CNS inflammation.
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Using a variety of CNS injury and mouse Alzheimer’s models, the role of HMGB1 will be examined using immunocytochemistry and computer analyses, RNA levels for inflammatory molecules will be quantified using real time RT-PCR methods, and inflammatory proteins will be determined using either western blot or ELISA. The experiments will involve inhibition of HMGB1 and its receptor using both injection of antibodies or gene therapy of natural antagonists. This experiments will shed light on the role of HMGB1 in CNS trauma, CNS vascular disease, and in Alzheimer’s disease. Read more
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Gary D. Paige, M.D., Ph.D.
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- Multisensory Interaction and Adaptive Plasticity in Spatial Localization and Orientation.
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The sensori-neural processes underlying our abilities to localize, track, and interact with a cluttered environment are crucial attributes of daily life, and are among the most fundamental tasks of the nervous system. The integration of multiple sensory inputs are required to guide spatial behaviors, ranging from mundane tasks such as reaching for objects, and complex ones such as navigating to and from the cafeteria for lunch. The goal of our research is to understand how the brain integrates sensory inputs from the outside world (location and motion of visual and auditory targets) with those of the internal senses (vestibular and somatosensory depictions of orientation and motion of the body and its parts,) to achieve meaningful spatial perceptions and behaviors (eye, head and postural movement). An equally important interest is how plastic neural mechanisms register errors and adaptively adjust performance in order to maintain proper spatial calibration across sensory modalities. Finally, an important translational concern is how the neural degeneration of natural aging affects spatial behavior and plasticity. Our research environment is unique in structure and instrumentation, as well as broad and translational in character. We benefit from a collegiate and multi-disciplinary group of faculty working on problems of common interest. Read more
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David B. Parfitt, Ph.D.
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- Early Life Stressors and Brain Development
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Our research examines the effects of early life stressors on brain development in the mouse. Students would be involved in raising mice under a variety of different rearing conditions and assessing behavioral, hormonal, and neurochemical stress reactivity in the adult offspring. Read more
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Tatiana Pasternak, Ph.D.
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- Neural mechanisms underlying working memory for visual motion
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The ability to briefly store visual information is fundamental to successful execution of visually guided behaviors. Research in my lab is aimed at the study of the circuitry underlying the active maintenance of the representation of sensory information, i.e. sensory working memory. The overriding goal is to provide a link between cortical areas traditionally associated with processing of visual motion (area MT) and the region identified with cognitive control of visually guided behaviors, prefrontal cortex and relate neural activity recorded in these two regions to perceptual decisions. Students rotating in the lab will have an opportunity to become familiar with procedures involved in neurophysiological recordings from behaving monkeys, including behavioral training techniques, single-cell recordings, analysis of neuronal activity, approaches to the study of behavioral effects of microstimulation and inactivation of identified cortical regions. They will work closely with other lab members and participate in the lab's weekly Journal Club. Read more
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David A. Pearce, Ph.D.
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- Characterization of the neurodegenerative mechanisms that underlie Batten disease using mouse models.
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Functional characterization of the CLN-proteins that are mutated in Batten disease. http://dbb.urmc.rochester.edu/labs/pearce/index.htm Read more
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Raphael Pinaud, Ph.D.
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- Molecular and cellular mechanisms of experience-dependent plasticity and sensory learning.
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A remarkable property of the vertebrate brain is that both its structural and functional connectivity is malleable and can adapt to alterations in the sensory environment. This intrinsic adaptive capacity, commonly referred to as plasticity, is required for normal brain development, learning, memory formation, and the response of the nervous system to central or peripheral damage. Work in my laboratory is focused on understanding the molecular and cellular basis of experience-dependent plasticity of sensory systems. In addition, we are interested in how normal and abnormal sensory experiences impact sensory perception, behavioral learning and memory formation. We use two experimental models to pursue these questions; the songbird auditory system and the rodent visual system. In both sensory systems we study a series of fundamental issues including (a) characterizing the anatomical and functional organization of circuits underlying sensory processing in these systems; (b) studying the impact of manipulations in the external environment (e.g., enhanced or deprived sensory experiences), or those intrinsic to the brain (e.g., genetic, pharmacological interventions or injury), and characterizing how these plasticity-inducing conditions impact sensory processing, learning and memory formation; (c) uncovering the molecular cascades that mediate these experience- and injury-induced plasticity events, and detailing how they are dynamically regulated; (d) establishing the precise roles that plasticity-related molecules play in modifying the physiology of single cells and neuronal ensembles to generate adaptive neural responses and behavior. To address the broad research lines outlined above, the Pinaud Lab employs a multi-disciplinary approach that involves rigorous molecular, cellular, anatomical and histological techniques, in addition to in-vitro electrophysiology (patch-clamp) and in-vivo multi-electrode recordings (awake animals). We also use high-throughput molecular screening strategies, including quantitative proteomics (2D-DIGE-based proteomics and mass spectrometry) and genomics approaches, in combination with behavioral methodologies. Finally, to establish causal links between experience-regulated molecular cascades and the physiology of neural circuits and behavior, we have been using knock-out and transgenic animal lines, and developing gene manipulation tools. The long-term goal of our research is to uncover how experience impacts the molecular and cellular biology of neurons and how these changes lead to altered neural processing strategies of behaviorally-relevant sensory information, ultimately leading to adaptive behaviors such as learning. Our research is also expected to shed light on potential ways to harness and/or alter the intrinsic molecular and cellular machinery of neurons to promote and facilitate functional recovery of sensory loss and a number of other disabilities that follow peripheral or central nervous system injury, such as deafness, blindness, phantom limb sensations and stroke. Read more
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Douglas Portman, Ph.D.
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- Genetic control of sex-specific behavior in C. elegans
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C. elegans is perhaps the only organism in which systems-level analysis of behavior and circuits can be connected to molecular genetic studies of neural development and function. Our laboratory is interested in understanding how sex-specific modification of the nervous system generates sexually dimorphic behaviors. We have recently found surprising and previously uncharacterized sex differences in olfactory and locomotory behaviors in C. elegans. A rotation student could further investigate some aspects of these or other behaviors with the ultimate goal of understanding their genetic and neuroanatomical underpinnings. Because little is known about how sex differences in the nervous system influence behavior and sensitivity to pathological insult in humans, this work has the potential to identify conserved pathways that mediate these process in all animals. Read more
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- Cell fate specification in the C. elegans nervous system
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The nematode C. elegans is a powerful invertebrate model for studying the conserved genetic programs that generate the tremendous cellular diversity of the nervous system in all animals. We are focusing on the development of a set of sensory structures called rays that innervate the adult male tail. Each ray is a simple three-celled sensillum that contains two sensory neurons and a glial-like cell. Read more
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David Rempe, M.D., Ph.D.
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- Hypoxia induced signaling in the brain and its impact on disease.
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The principle focus of Dr. Rempe’s laboratory is examining hypoxia induced signaling mechanisms in the brain and their impact on cell viability during disease, especially stroke. In particular, we are interested in the role of the HIF transcription factors in astrocytes and neurons and its impact on neuronal viability during hypoxic stress. To this end, we are utilizing cells derived from transgenic mice with conditional loss of HIF-1a function. Using in vitro and in vivo approaches, we examine loss of HIF-1a function in astrocytes or neurons to examine cell-type specific effects. To date, we have demonstrated that loss of HIF-1a function in astrocytes markedly abrogates hypoxia induced neuronal cell death in vitro. This HIF-1a mediated pathological function in astrocytes was unexpected and points to an unappreciated and important role of HIF-1a function within astrocytes on neuronal viability during hypoxia. The molecular mechanisms by which this pathological function of HIF-1a is mediated are a focus of investigation. Read more
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- Characterizing the function of a novel HIF-1 target identified by micro-array analysis
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A second focus of Dr. Rempe’s laboratory includes characterizing the function of a novel HIF-1a target that was identified by micro-array analysis. The target is of particular interest because of a mitochondrial localizing signal within its amino-terminus. Preliminary work has confirmed its mitochondrial localization. While the function of the protein is still unknown, overexpression of this protein induces marked changes in mitochondrial morphology causing a collapse of the normally diffuse mitochondrial network into a large peri-nuclear clustering of the mitochondria in astrocytes. Furthermore, EM studies demonstrate dilation of matrix and condensation of cristae associated with overexpression of this hypoxia-induced protein. The impact of this new HIF-1a target on mitochondrial function is now being explored. Read more
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Patricia M. Rodier, Ph.D.
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- The embryology of autism
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The present focus in the lab is on the etiologies of autism. This neurodevelopmental disorder can be caused either by exposure to toxic agents or by genetic abnormalities. We have proposed that the key to understanding how the same disorder can arise from disparate causes is that the timing of the injury to the embryo is the same in both cases. We know that some of the teratologic cases are due to insults during neural tube closure. One of these exposures, valproic acid, has been used to create an animal model that parallels human autism in both neuroanatomy and behavior. Mutations of some of the early developmental genes active at the same developmental stage are good candidates for explaining familial cases of autism. The anatomical phenotype in humans is similar to that of mice transgenic for null mutations of several early developmental genes, especially HOXA1, a gene involved in one of the genetic syndromes that include autism as a feature. Read more
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Lizabeth M. Romanski, Ph.D.
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- Audiovisual integration in the primate prefrontal cortex
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Rotation will involve assisting in daily recording sessions with rhesus macaques trained in a memory task involving short movies of monkey vocalizations. We will record from single neurons in the ventral prefrontal cortex and determine the neuronal response to congruent and incongruent face and vocal stimuli. Daily activities will include training and handling of macaques, team recording sessions, data entry and review and data analysis. Read more
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- Projections to auditory, visual and multimodal responsive regions of the prefrontal cortex
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Rotation will focus on analyzing the connections of the prefrontal cortex with other cortical association regions involved with auditory and visual processing. We have previously placed anatomical tracers into auditory and visual prefrontal regions. In this rotation we will process these cases using standard histological techniques and immunocyotochemical localization of several tracers including fluoro-ruby, fluoro-emerald, Lucifer yellow and fast blue. After the sections have been processed and photographed the resulting retrograde cells and anterograde fibers will be charted using the digitizing program NeuroLucida. All images will be summarized via 3-D reconstructions so they are publication-ready. Read more
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Duje Tadin, Ph.D.
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- Neural mechanisms of visual perception
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We use psychophysics, transcranial magnetic stimulation (TMS), fMRI, and eye-tracking to investigate neural mechanisms of visual perception in normal and special populations. Current topics include motion perception, binocular rivalry, visual awareness, contextual interactions, perceptual learning, visual adaptation, attention and temporal dynamics of vision. For example, our psychophysical work has revealed several counterintuitive characteristics of human motion perception and linked these findings with cortical center-surround mechanisms. Follow-up work investigated temporal and spatial properties of center-surround interactions across visual sub-modalities in normal, schizophrenic and MDMA-user populations. Another line research relies on binocular rivalry and visual crowding as experimental methods for studying the characteristics of visual awareness. Read more
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Michael Weliky, Ph.D.
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- Population neural activity in the visual system
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We are interested in mechanisms of sensory processing and perception in awake animals, as well as their emergence during brain development. We use multi-electrode recording (up to 64 electrodes) to study the interaction between ongoing activity and sensory input signals across single and multiple visual areas, and use computer modeling to help interpret and analyze our data. Read more
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