University of Rochester Medical Center

Available Lab Rotations

Announcement Length

 
 
Principal Investigator Rotation
William J. Bowers, Ph.D. Photo of William Bowers
Novel modeling of Alzheimer's disease/inflammation interactions
Novel anatomically and temporally controlled inflammation mouse models are being created, that when combined with an established mouse model of Alzheimer's disease (AD), will be utilized to elucidate the role of brain inflammation in propagation of AD-related pathogenesis and how peripheral vaccination modulates this process. Quantitative bionomic technology will be used in parallel with standard histochemical, biochemical, and electrophysiological assays to correlate the molecular mechanisms by which inflammation influences the initiation and propagation of AD-like pathology and degradation of hippocampal-associated synapses. Read more For specific questions, please contact me via email.
Gene therapeutic strategies for neurodegenerative diseases
Herpes simplex virus (HSV)-derived amplicon vectors are being optimized for the treatment of neurodegenerative diseases arising early in life. For this project, novel integration-competent forms of the amplicon are being created that will direct expression of gene products specifically within neurons and neuroprogenitor cells of the brain. These studies will yield a novel HSV vector platform, provide a detailed understanding of transgene expression in vivo, and evaluate the therapeutic effectiveness of protecting neurons in well-established models of disease. Read more For specific questions, please contact me via email.
Laurel H. Carney, Ph.D. Photo of Laurel Carney
Auditory Neuroscience
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.
Greg DeAngelis, Ph.D. Photo of Greg DeAngelis
Neural mechanisms of depth perception
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 For specific questions, please contact me via email.
Sensory integration for self-motion perception.
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 For specific questions, please contact me via email.
Edward G. Freedman, Ph.D. Photo of Edward Freedman
Neural Control of Coordinated Movements
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 For specific questions, please contact me via email.
Robert S. Freeman, Ph.D. Photo of Robert Freeman
Mechanisms of neuronal cell death in development and disease
During development of the nervous system as many as half of all neurons produced by neurogenesis are eliminated by a process known as programmed cell death. Much of this cell death occurs as neurons extend axons to their targets and compete for limiting amounts of survival-promoting neurotrophic factors, such as nerve growth factor (NGF). The selective elimination of neurons at discrete points in development is critical for sculpting a properly functioning nervous system. In the mature nervous system, however, genetic and/or environmental factors that cause too much or too little cell death can lead to a variety of human pathologies ranging from Alzheimer’s disease to brain cancer. From evidence accumulated over the last 20 years, we now know that these pathological cell deaths and the cell deaths that occur normally during development share similar morphological and biochemical features. Research in my laboratory is aimed at understanding the molecular mechanisms that regulate cell death in the nervous system. More specifically, we strive to identify and characterize critical cell signaling events that, if left unchecked, eventually commit a neuron to die. Currently, we are attempting to uncover the mechanisms by which two proline-modifying enzymes, the oxygen and iron-dependent prolyl hydroxylase EGLN3 and the peptidyl-prolyl isomerase Pin1, function to regulate cell death in neurons deprived of NGF. Other research interests include determining the effects of hypoxia on programmed cell death and investigating the mechanisms by which hypoxia-inducible transcription factors promote survival in neurons. In our studies we apply the techniques and approaches of cell biology, molecular biology, genetics, and biochemistry to both in vitro and in vivo model systems. As basic science researchers, we are driven by the prospect that the mechanisms we uncover will someday contribute to the development of novel therapies for cell death-related diseases and disorders of the nervous system. Read more For specific questions, please contact me via email.
Lin Gan, Ph.D. Photo of Lin Gan
Transcription factors in neurogenesis
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 For specific questions, please contact me via email.
Harris A. Gelbard, M.D., Ph.D. Photo of Harris Gelbard
Glial and immune effector cell interactions with synapses during neuroinflammation
To use Al Gore's words, NeuroAIDS remains an inconvenient truth. Despite the fact that highly active antiretroviral therapy (HAART) has made AIDS a chronic, treatable disease, it has proven considerably less effective as a therapy for the neurologic disease associated with HIV-1 infection of the central nervous system (CNS), despite its ability to drive viral load to undetectable levels. With over one million people infected with HIV-1 in the U.S. and well over 40,000,000 people infected worldwide, HIV-1's ability to enter the CNS early in the course of infection, makes it a major source of neurologic morbidity, especially in a population that is aging and beginning to experience other neurodegenerative diseases, including Alzheimer's and Parkinson's disease. Because HIV-1 infects cells of mononuclear lineage, but not post-mitotic neurons, it disrupts normal CNS functions by the production and secretion of pro-inflammatory cellular metabolites and viral gene products that act as neurotoxicants. Our laboratory has investigated the effects of these neurotoxins on normal immune effector functions in the CNS as well as synaptic function. Our working conclusion is that initial infection with the virus in the CNS leads to a change in the functional phenotype of immune effector cells, leading to chronic neuroinflammation and failure of synaptic communication. In particular, we have focused on how HIV-1 neurotoxins disrupt the normal function(s) of two enzyme targets, glycogen synthase kinase 3 beta (GSK-3β) in neurons, and mixed lineage kinase 3 (MLK3) in neurons and perivascular macrophage/microglia, with the ultimate goal of designing small molecule therapies to prevent their pathologic over-activation by inflammatory neurotoxins. As part of this collaborative effort between several labs at our institution, we utilize standard in vivo multiphoton microscopy of cortical window preparations in transgenic mice as well as novel optical imaging techniques to better understand nano-scale changes that occur to synaptic architecture during inflammation, as well as gain insight into how cells with immune effector functions can directly effect synaptic transmission. We do this with the goal of determining what the bioenergetic consequences of synapse remodeling are in the face of immune activation, and whether inflammation inevitably leads to loss of functional synaptic architecture with the ability to retain plasticity. Read more For specific questions, please contact me via email.
Joseph Christopher Holt, Ph.D. Photo of Joseph Holt
Cellular and Molecular Mechanisms of Synaptic Transmission in the Vestibular Periphery
Many sensory systems are endowed with efferent feedback mechanisms that can modulate their primary input to the brain. That is, incoming information from a peripheral detector is delivered to a way station within the CNS which then modifies the output from that same detector. Everyday examples include the pupillary reflex to bright light entering the eyes, the contraction of middle ear muscles to loud sounds, or the recruitment of additional muscle fibers when first lifting a heavy object. Here, the function of the efferent loop is presumably to optimize or “tune” each sensory modality to its stimulus. Sensory information regarding the position and movement of the head are encoded by the vestibular system, which begins as a number of small detectors located within the inner ear. Like the preceding examples, the peripheral vestibular system is also endowed with a prominent efferent innervation. The functional role of this feedback system, however, is relatively unknown. We do know that when these efferent pathways are electrically stimulated, afferent output from vestibular endorgans is profoundly inhibited or excited, suggesting that vestibular efferents may be involved in both negative and positive feedback. If such efferent activity occurs under physiological conditions, it is almost certain to modify and transform vestibular information traveling to the CNS. Yet, very little information is available as to how and when these efferent actions ultimately impact the processing of vestibular information in an alert animal. Taking a reductionistic approach, my lab is addressing the function of the vestibular efferent system from three vantage points: (1) Identifying the receptor mechanisms by which different efferent responses are generated during activation of their pathways; (2) Characterizing how these efferent receptor mechanisms modulate afferent response properties by pairing afferent recordings during vestibular stimulation with activation of efferent pathways; and (3) Identification of efferent discharge patterns with direct, in vivo recordings from vestibular efferent neurons. Such knowledge is critical in evaluating efferent function in behaving animal models, one of our long term goals. Students rotating in the lab can learn neurophysiological, pharmacological, and immunohistochemical methods for studying vestibular synaptic transmission in several animal models, and the necessary computational techniques for analyzing these data. Read more For specific questions, please contact me via email.
Gail V. W. Johnson Voll, Ph.D Photo of Gail Johnson Voll
The role of tau and mitochondrial dysfunction in the pathogenesis of Alzheimer’s disease
A predominant neuropathological hallmark of Alzheimer’s disease is the neurofibrillary tangle which is formed by an abnormally modified form of the tau protein. Tau is a microtubule-associated protein that is primarily neuronal and plays an essential role in microtubule-based processes. In Alzheimer’s disease, tau becomes abnormally modified and aggregated, which leads to neuronal dysfunction and death. In our lab we are interested in how specific modifications of tau lead to its dysfunction and accumulation. In particular we are presently investigating the role of chaperones in regulating tau turnover, the role of site-specific phosphorylation in regulating tau aggregation and degradation and how abnormally modified tau impairs mitochondrial function. In this lab we use a wide range of molecular, cell biological and imaging techniques. Although we primarily use cell models (both clonal and primary), we are now examining tau processing and turnover, as well as toxicity due to abnormal processing in vivo using C. elegans as model system. There are many exciting opportunities for rotation projects on tau in my laboratory. Read more For specific questions, please contact me via email.
Understanding the mechanisms of tau toxicity in Alzheimer disease
The focus of our studies is on understanding how Alzheimer disease (AD)-relevant forms of tau impair neuronal function. Pathological modifications of the tau protein occur prior to the clinical manifestation of AD. Tau is likely a mediator of A toxicity that occurs in AD, due in part to abnormal posttranslational modifications of tau, particularly phosphorylation and C-terminal cleavage. AD-relevant posttranslational modifications of tau alter tau conformation, which negatively impacts its interactions with other proteins (as well as itself), and thus could ultimately contribute to neuronal impairment. Mitochondrial dysfunction is likely a prominent player in the pathogenesis of AD, as substantial evidence demonstrates that aberrant mitochondrial metabolism and localization contribute to synaptic dysfunction and loss. Since it is clear that modifications of tau and compromised mitochondrial biology are early events in AD, the crucial questions are, 1) What is the effect of pathological forms of tau on mitochondrial biology and, 2) What are the mechanisms involved? We have demonstrated that expression of an AD-relevant, truncated form of tau (tau-D421) in neuronal cell models results in increased mitochondrial fragmentation, dysregulation of calcium uptake by mitochondria, and loss of mitochondrial membrane potential (m) in response to pathological increases in intracellular calcium in comparison to cells which inducibly express wild type tau. In addition, even under basal conditions, expression of tau-D421 significantly increases the number of fragmented mitochondria and production of reactive oxygen species (ROS) in comparison to expression of wild type tau. These findings indicate mitochondria are a target of pathological tau. Overall the studies in our lab are focused on examining the mechanisms by why pathological forms of tau negatively impact neuronal survival. Read more For specific questions, please contact me via email.
Ania K. Majewska, Ph.D. Photo of Ania Majewska
Mechanisms of Plasticity in the Visual System
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 For specific questions, please contact me via email.
Manipulating neurons during epileptic activity in hippocampal slices
Epilepsy is a devastating disease and current treatments are complicated by many side effect. Controlling the firing of specific types of neurons during an epileptic seizure could allow a side-effect free treatment for this condition. We are currently using optogenetic methods to control the activity of hippocampal neurons in brain slices. Light-sensitive proteins are delivered to specific neurons using viruses. These proteins hyperpolarize or depolarize the neuron when light is provided. We are examining whether epileptiform activity in acute rat slices can be altered using light activation of these proteins. A rotation in the lab would expose students to rodent surgeries, acute slice preparation, electrophysiology and immunocytochemistry. Read more For specific questions, please contact me via email.
Brain activity and breast tumor metastasis to the brain
Many breast cancer patients develop neurological side effects such as depression, chemobrain, or epilepsy. To manage these side effects, many neurological agents are currently prescribed to breast cancer patients either prophylactically or in response to symptoms without a clear understanding of how these may affect metastasis. We are currently examining how these neurological agents alter breast tumor metastasis to the brain in a mouse model and whether brain activity plays a role in affecting tumor penetration into the brain and subsequent growth. A rotation in the lab would expose students to rodent surgeries, cell culture, histology and immunocytochemistry. Read more For specific questions, please contact me via email.
Margot Mayer-Pröschel, Ph.D. Photo of Margot Mayer-Pröschel
Animal model development for autism
Animal model development for autism Read more For specific questions, please contact me via email.
Influence of smoking on brain function
Influence of smoking on brain function Read more For specific questions, please contact me via email.
Impact of anesthesia of brain function
Impact of anesthesia of brain function Read more For specific questions, please contact me via email.
Role of iron in embryonic development
Role of iron in embryonic development Read more For specific questions, please contact me via email.
Mark Noble, Ph.D. Photo of Mark Noble
CNS stem/progenitor cell biology; stem/progenitor cell physiology; redox biology; toxicology/disease; cancer stem cell biology
Students rotating in our laboratories have the opportunity to partake in a wide range of projects pertaining to our goal of making rapid progress on numerous components of the field of stem cell medicine. The overarching theme of our work is to understand what the field of stem cell medicine will look like 20-30 years in the future, and then speed progress along these paths. Our laboratory members work on projects that include cell discovery, fundamental mechanisms underlying the control of division and differentiation, the contribution of intracellular redox state to regulation of cell function, repair of CNS damage, numerous neurological diseases, toxicology and cancer biology. Rotation opportunities exist in most of the areas in which we work, thus providing opportunities to work on a continuum of projects that span the territory from basic scientific research to clinical implementation of therapeutically promising discoveries. Read more For specific questions, please contact me via email.
Gary D. Paige, M.D., Ph.D. Photo of Gary Paige
Multisensory Interaction and Adaptive Plasticity in Spatial Localization and Orientation.
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 For specific questions, please contact me via email.
Tatiana Pasternak, Ph.D. Photo of Tatiana Pasternak
Neural mechanisms underlying working memory for visual motion
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 For specific questions, please contact me via email.
Raphael Pinaud, Ph.D. Photo of Raphael Pinaud
Molecular and cellular mechanisms of experience-dependent plasticity and sensory learning.
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 For specific questions, please contact me via email.
Douglas Portman, Ph.D. Photo of Douglas Portman
Genetic control of sex-specific behavior in C. elegans
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 For specific questions, please contact me via email.
Neural and genetic control of sex differences in C. elegans behavior
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 For specific questions, please contact me via email.
David Rempe, M.D., Ph.D. Photo of David Rempe
Hypoxia induced signaling in the brain and its impact on disease.
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 For specific questions, please contact me via email.
Defining the function of HUMMR, a hypoxia induced protein that alters mitochondrial transport.
A second focus of Dr. Rempe’s laboratory includes characterizing the function of a novel HIF-1a target (HUMMR) that was identified by micro-array analysis. The target is of particular interest because it localizes to mitochondria and alters mitochondrial transport. Overexpression of HUMMR 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, loss of HUMMR function enhances mitochondrial movement in hypoxia, but not normoxia. Since alterations in mitochondrial transport alter synaptic plasticity and are identified in a number of diseases, including Alzheimer’s disease and hypoxia/ischemia, we are examining the impact of HUMMR on neuronal plasticity during diseases states such as stroke. Read more For specific questions, please contact me via email.
Patricia M. Rodier, Ph.D. Photo of Patricia Rodier
The embryology of autism
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 For specific questions, please contact me via email.
Lizabeth M. Romanski, Ph.D. Photo of Lizabeth Romanski
Encoding and integration of faces and vocalizations in the frontal lobe of primates
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 For specific questions, please contact me via email.
Anatomical circuits that convey auditory and visual information to the frontal lobe
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 For specific questions, please contact me via email.
Duje Tadin, Ph.D. Photo of Duje Tadin
Neural mechanisms of visual perception
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 For specific questions, please contact me via email.