Neuroscience Program Faculty
The Brunken lab researches the influence of the environment in regulating brain and ocular development, and its dysregulation in disease. Our areas of interest include epigenetic regulation and the role of cell-extracellular matrix interactions. Using cell culture and mouse models, we are able to identify molecular mechanisms of developmental regulation. Professor Brunken is the Director of the Center for Vision Research.
The Calancie lab researches mechanisms of central nervous system plasticity following trauma, with a particular focus on spinal cord injury. We use intraoperative electrophysiology to assess neuronal signaling directly following spinal cord injury. Our clinical work includes the validation of neuromonitoring techniques for use in surgical interventions in and around the spinal cord.
The Calvert lab researches the molecular mechanisms which dictate signal-dependent protein localization and transport. Our work focuses on protein transport and localization in photoreceptor neurons, which have highly regulated transport of proteins between different compartments. When disrupted, these systems have the potential to cause retinal degenerative diseases.
The Chen lab researches mitochondrial biology and stress signaling, with a focus on mechanisms of aging-dependent muscle wasting and neuromuscular diseases. While mitochondrial dysfunction plays a role in these diseases, the underlying mechanisms are poorly understood. We use yeast, cultured human cell lines and mouse as model systems, to identify molecular pathways with the potential to delay or reverse mitochondria-induced cellular degeneration.
The Faraone lab researches the genetic and molecular pathways associated with ADHD and various neurodevelopmental disorders, including improving diagnosis and treatment of ADHD. Because ADHD is also linked with aggressive behavior, substance use disorders, and mood/anxiety disorders, the Faraone lab seeks to identify genes and genetic risk factors related to these diagnoses using machine-learning techniques, genome-wide association studies, and through international collaborations.
The Glatt lab has multiple research projects aimed at finding the genetic and environmental risk factors for a wide variety of disorders, including schizophrenia, bipolar, post-traumatic stress, Alzheimer's disease, and substance abuse. We seek to identify "risk genes" for these disorders by studying affected individuals and families. Ultimately, we hope to develop interventions which can treat or prevent these disorders.
The Hu laboratory studies mechanisms of retinal degeneration in the blinding disease retinitis pigmentosa and of brain malformations in syndromic congenital muscular dystrophies associated with development delays and ocular abnormalities. We use the zebrafish and mouse to model these human disorders. Currently, we are developing experimental gene therapies using various animal models.
The Knox lab researches the regulation of gene expression during ocular development and cell differentiation. Our particular focus is on the transcriptional regulation of the rod photoreceptor protein rhodopsin. Using techniques such as the yeast one-hybrid assay, we identify potential transcription factors of rhodopsin, which we then test in downstream analyses to fully characterize the molecular dynamics involved in the regulation of this critical visual system gene.
Dr. Licinio currently serves as the Senior Vice President for Academic Health Affairs & Executive Dean, and Dean of the College of Medicine at SUNY Upstate Medical University. He is well known for his research into leptin and its role in conveying a feeling of satiety. In more recent work, Licinio and collaborators have examined the effects of the human microbiota and the microbiome-gut-brain (MGB) axis in obesity with diabetes and on behaviors relevant to depression and schizophrenia, an area which opens potentially novel avenues for the treatment of psychiatric disorders.
Research in the Liu lab mainly focuses on identifying the molecular mechanisms of of major psychiatric diseases, particularly bipolar disorder and schizophrenia. We use comprehensive approaches, including genetics, bioinformatics, genomics, and cellular & animal models.
Research in the Lin lab focuses on exploring cellular and molecular mechanisms by which experience is coupled to modifications of neural circuits that lead to long-term behavioral changes, with ongoing projects in the four major areas: 1) Molecular and circuit mechanisms of learning and memory; 2) Neural circuit assembly and synapse development; 3) Molecular and circuit mechanisms of neurological disorders; and 4) Neurogenetic tool development. The Lin lab conducts their research using multi-disciplinary approaches, including molecular & cellular biology, mouse genetics, electrophysiology, imaging, chemogenetics, optogenetics, and mouse behavior.
The Massa lab researches inflammation of the central nervous system with a focus on Multiple Sclerosis. Our major goal is to identify the biological determinants of pathological changes which lead to MS by focusing on immune cell activation and infiltration of the central nervous system. In order to accomplish this, we combine patient cell and mouse models of MS. In particular, we examine gene expression and its determinants using a combination of techniques, which include bisulfite sequencing, reverse transcription PCR, Western blotting, and more.
The Matthews lab studies the role of extracellular microenvironment in normal brain development and maturation, and its contribution to neural disorders and injury. Our lab is particularly interested in a substructure within the extracellular matrix called the perineuronal net. This structure is a key regulator of developmental plasticity and has been implicated in an array of neuropsychological and neurological disorders. The lab utilizes a combination of biochemical, neuroanatomical, and molecular approaches to understand the function of perineuronal nets and the neural extracellular matrix in both the normal and damaged brain.
The Middleton lab is focused on determining the biological bases of psychiatric and neurological disorders. We use high-throughput genetic, epigenetic, and functional genomic techniques with human subjects or animal and cellular models to identify molecular mechanisms linked to these disorders. We are particularly interested in autism, schizophrenia, ADHD, Parkinson's disease, alcohol abuse, and traumatic brain injury. Dr. Middleton is the Director of the Neuroscience Graduate Program at SUNY Upstate Medical University.
Research in the Motter lab examines the neural correlates underlying visual perception and attention in primates. Recent efforts have focused on the study of neurons in prestriate cortical area V4 during visual search and free search conditions. Two major projects concern defining the contribution of saccadic momentum (an oculomotor bias toward making a saccade in the forward direction relative to a previous saccade) and modeling how neurons in V4 contribute to overcoming the constraints on peripheral object perception in cluttered visual scenes (termed visual crowding).
The Olson laboratory studies neurodevelopmental disorders that disrupt dendritic initiation and growth. The dendrite is a major component of the wiring of the brain, and disruptions of dendritic development are associated with profound intellectual disability and epilepsy. We use multiphoton microscopy and mouse disease models to examine how genetic mutations, early neural activity and environmental factors affect dendritic growth and brain structure.
The Pignoni lab focuses on the roles of transcription factors and signaling molecules in neurogenesis and eye development. We primarily use the Drosophila melanogaster as an in vivo model, as it provides us with an incomparable platform for genetic analyses. We also work in cell culture and in yeast to dissect protein function at a molecular level. Lastly, we rely on transcriptomics to understand gene networks. Genes we study are cause of congenital disorders in humans. Dr. Pignoni currently serves as the Interim Chair of Neuroscience & Physiology.
The Solessio lab applies electrophysiological techniques, animal visual behavior, and mathematical modeling to identify the cellular and molecular mechanisms of temporal processing in the retina. We recently developed an operant assay where mice are trained to detect and respond to a flickering visual stimulus, an action that requires cortical input and decision-making. Using this approach, we have established a model of vision that matches fundamental properties of human psychophysics. We are currently pursuing two lines of research using different transgenic mouse lines: 1) determine how photoreceptor kinetics shape visual temporal information as the retina transitions seamlessly between rod-driven vision in dim lights and cone-driven vision in bright lights, 2) determine the limitations in the processing of temporal visual information in common forms of retinal degeneration.
The Ts'o lab is interested in decoding the underlying logic of cortical region development, particularly in cases where multiple regions share a common purpose, or a common region serves multiple functions. Our studies have revealed different pathways for distinct aspects of visual processing in a patchwork map of the cortex. In the visual cortex, we are studying how the various visual cortical regions interact. In the neocortex, we study how functional domains can be segregated within a cortical region. Together, these studies have important implications for our understanding of the brain's architecture and connectivity.
Modification of synaptic neurotransmission at glutamatergic synapses and activation of Ca2+-dependent second messenger systems contribute to the processes of learning and memory, neuronal survival and differentiation. These systems play important roles in the neuronal dysfunction that is observed following stroke and ischemia, focal epilepsies, and Alzheimer’s disease. The Vallano lab is focused on analysis of the expression and functional responsiveness of distinct excitatory amino acid receptors (NMDA subtypes), modulation of responses by Ca+2-dependent protein kinases, and examination of the roles of these receptors and kinases in neuronal survival and differentiation.
The Viapiano laboratory studies the mechanisms by which the neural microenvironment contributes to brain cancer initiation and growth. In particular, we focus on extracellular matrix components that trigger pro-tumoral effects and are produced by cancer cells. We generate novel reagents to target these molecules in brain cancer and utilize patient-derived and organ-on-chip tumor models; mouse models of cancer; molecular and cellular techniques; and high-end genomic analyses of brain cancer datasets and biopsy samples to develop new diagnostic and therapeutic strategies.
The Viczian lab is interested in human eye disease and how it originates during embryonic development. This process is disrupted in patients with anophthalmia (no eye) and microphthalmia (small eye), where the underlying cause in many cases is unknown. We identified T-box transcription factor, Tbx3, as an initiator of eye formation in frog. Our lab has extended these studies to the mouse, where we will determine which stages of mammalian retinal development require Tbx3. When misregulated, Tbx3 causes cancer. In other areas of the body, Tbx3 is required for normal lung, heart, limb and mammary gland formation. How Tbx3 is regulated in the eye and its underlying function is unknown. Insight into how this transcription factor functions may reveal links to causes of developmental eye disease.
The MiNDS lab uses quantitative molecular biology and neuroanatomical techniques in the postmortem human brain and in animal models to understand the biological basis of schizophrenia. In order to understand normal human development and aging, we chart molecular and cellular brain changes across the human life span, in humans from two months in age to 100 years. Using cellular neurobiology, histology, anatomical molecular mapping, transcriptomics, and quantitative molecular assays of proteins, metabolites and enzyme activity to analyze the human cortex and basal ganglia, we seek to uncover the underlying causes of schizophrenia and other disorders.
The Cognitive Neuroscience of Schizophrenia Laboratory aims to expose the relationships between thought impairment, genetic influence, and brain dysfunction in people with schizophrenia. Our translational research uses molecular findings from our collaborators to identify novel treatment targets. We combine brain imaging (MRI/fMRI/DTI), cognitive testing, genetic testing, and analysis of molecular biomarkers to validate and repurpose existing medications as adjunctive treatments in schizophrenia.
The current research focus of the Wojcikiewicz lab is the degradation of IP3 receptors and other endoplasmic reticulum proteins by the ubiquitin-proteasome pathway. We are particularly interested in novel proteins and mechanisms that mediate endoplasmic reticulum protein degradation. Dr. Wojcikiewicz currently serves as the Chair of Pharmacology.
The Wong lab researches major depressive disorder (MDD) and comorbid diseases using a combination of animal models and clinical studies. We look at MDD at both a systemic level, investigating the relationship between MDD and the gut microbiome in animal models; and at a cellular level, characterizing the role of the inflammasome and novel targets in mediating stress-induced depressive-like behavior and antidepressant response. We have also been probing the role of glia in eating, anxiety, and depressive behaviors. Our lab is very collaborative, both within Upstate Medical University and with external investigators.
The Yao lab researches neuronal connectivity deficits in psychiatric disease. Using mouse models and patient-derived stem cells, we investigate how impaired assembly, function, and plasticity of synapses contribute to the cognitive and emotional deficits of psychiatric illness. Using molecular biology and electrophysiology, we have identified new brain signaling pathways which regulate synapse formation, stabilization, and rewiring. These breakthroughs provide a foundation for further cutting-edge research into synaptogenesis and synaptic plasticity in addiction, schizophrenia, autism, and other prefrontal cortex-related diseases.
The Zhao lab investigates the mechanisms underlying pathological progression and brain repair in cerebrovascular diseases, brain trauma, and neurodegenerative diseases. Our long-term goal is to search for new strategies for enhancing brain repair in stroke and traumatic brain injury and for restricting pathological progression in Alzheimer’s disease and CADASIL disease. By recently recognizing that brain diseases and injuries disrupt the entire brain networks and brain functioning, Zhao lab research aims to develop next-generation approaches for brain repair in these devastating diseases. Current research projects in the Zhao lab are supported by research grants funded by the NIH and VA.
The Zhu lab is focused on characterizing processes of brain development using the Drosophila model. In type II neuroblast lineages, intermediate neural progenitors greatly expand production of neurons. By elucidating mechanisms underlying the proliferation and differentiation of the intermediate neural progenitor cells, we hope to gain mechanistic insights into the generation of brain complexity and brain tumor formation. In the mushroom body of the adult Drosophila brain, the mushroom body output neurons connect through their dendrites to specific axonal segments of mushroom body neurons. We use this model to clarify cellular and molecular mechanisms underlying subcellular-specific targeting of dendrites. Such subcellular specificity of synaptic connections has profound impact on neuronal activity and function.
Normal nervous system development requires the precise control of both cell proliferation and differentiation (neurogenesis). Diseases resulting in too few, the wrong type, or too many neural cells, all have devastating effects, including developmental defects, cancers, and abnormal brain function. The Zuber lab uses both frogs and mice to address the fundamental question, “How are proliferation and differentiation balanced in neural cells?” Our long-term goals are to determine how this balance is maintained and identify changes that disrupt normal neural differentiation. Answering this seemingly simple question could lead to treatments for human diseases resulting from premature or delayed neurogenesis.