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Neuroscience Program

Neuroscience investigators focus on:

  • The neural, molecular, and genetic mechanisms that underlie nervous system development, learning and memory, addiction, glial responses to neuronal injury, and circadian rhythmicity; 
  • Mechanisms of synaptic neurotransmitter release, analysis of how neurotransmitter receptors and membrane channels operate, and how drugs act on these processes to modify cellular function and behavior; 
  • Magnetic resonance imaging technology to study and map changes in the brain associated with physiological stimuli as well as drugs of abuse; and 
  • Disorders of the central nervous system, with special emphasis on neurodegenerative disorders, autism spectrum disorders, mental retardation and other developmental disabilities. 

REQUIREMENTS FOR SPECIALIZATION

All Basic Biomedical Science students must complete the core curriculum as well as electives required by their program. Students in the Neuroscience program must take 3 graded elective courses of 2-4 credits each, one of which must be Cellular, Molecular and Developmental Neuroscience, usually in the spring of the first year. Courses offered by other programs may be taken to complete the other elective requirements.

View PhD Program Schedule  |   View courses

OUR LEADERSHIP & FACULTY

PROGRAM DIRECTOR

David Weaver, PhD
Professor
email Dr. Weaver

OUR FACULTY

The Program in Neuroscience is interdepartmental, administered under the umbrella of the Department of Neurobiology. Participating faculty have primary appointments in several departments, with the largest concentration of faculty coming from the Departments of Neurobiology, Neurology, Psychiatry, MaPS, Medicine, and Molecular Medicine.

Neuroscience Program faculty listing

OUR STUDENTS

STUDENT EXPERIENCE

The program maintains a schedule of seminars and intramural research presentations that ensures a cohesive program. This atmosphere is especially conducive to the scientific growth of graduate students obtaining their degrees in neuroscience.

View current and past student listing

OUR STUDENTS IN THE NEWS

Getting Results…
  • PhD candidate finds dogs are perfect companion to understanding human health
    Education News

    PhD candidate finds dogs are perfect companion to understanding human health

    Kathleen Morrill, a PhD candidate in the Morningside Graduate School of Biomedical Sciences, has made national headlines for her research into behavioral traits of dogs.

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  • Lauren O’Connor receives prestigious NIH Kirschstein Award
    Education News

    Lauren O’Connor receives prestigious NIH Kirschstein Award

    PhD candidate Lauren O’Connor identified multiple bacteria that suppress degeneration in worms. She is investigating how they protect the nervous system and whether specific diets can protect against multiple models of neurodegeneration.

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  • UMass Chan biomedical sciences student studies a gene that causes ALS
    Education News

    UMass Chan biomedical sciences student studies a gene that causes ALS

    PhD student Megan Fowler-Magaw is researching the pathogenesis of ALS, using a specific gene that is found in 97 percent of cases.

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  • PhD candidate studies mental illness progression and alcoholism
    Education News, Media

    PhD candidate studies mental illness progression and alcoholism

    Jenya Kolpakova, a PhD candidate in the Graduate School of Biomedical Sciences’ neuroscience program, came to the United States from Ukraine when she was 15. She is studying changes in the brain due to binge alcohol drinking.

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  • From Kolkata to Worcester, GSBS student Kasturi Biswas drawn to science of the brain
    Education News, Media

    From Kolkata to Worcester, GSBS student Kasturi Biswas drawn to science of the brain

    Kasturi Biswas, a PhD candidate in neurobiology, traveled from her native India to Massachusetts to study at UMass Medical School.

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  • Kellianne Alexander named HHMI Gilliam Graduate Fellow
    Media, Research News

    Kellianne Alexander named HHMI Gilliam Graduate Fellow

    Graduate School of Biomedical Sciences student Kellianne Alexander has been awarded a Howard Hughes Medical Institute Gilliam Graduate Fellowship. Learn more about her research in this Women in Science video.

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EXTERNAL AWARDS FOR RESEARCH TRAINING (CURRENT)

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    Dissecting ADAM10 function in microglia-mediated synapse elimination

    The goal of this proposal is to dissect the molecular signaling between microglia and neurons that regulates synapse elimination in response to changes in sensory experience. Despite compelling evidence that microglia, the resident brain macrophages, play important roles in eliminating synapses in development and disease, the precise neuron-to-microglia molecular signaling that drives this process is poorly understood. I recently discovered a signaling pathway necessary for microglia-mediated synapse elimination by utilizing the well-described circuitry of the mouse barrel cortex circuit as a model to manipulate sensory experience and dampen neuronal activity. Here I found microglia robustly engulf synapses in the barrel cortex following either whisker lesioning or trimming, and that this engulfment is dependent on the microglial CX3CR1 receptor and its canonical neuronal ligand, CX3CL1, but not complement. Using single-cell RNAseq I also found that neuronal Cx3cl1 was not differentially regulated in the cortex following whisker removal, but the protease Adam10, known to cleave membrane-bound CX3CL1 into a soluble form, is increased following lesioning. Importantly, pharmacological inhibition of ADAM10 resulted in synapse elimination defects that phenocopied CX3CR1 and CX3CL1-deficient mice. These data suggest that post-translational modification of neuronal CX3CL1 by ADAM10 is required to regulate microglial synapse elimination in the cortex following whisker removal. Several exciting new questions have now arisen, which I will tackle in this proposal: 1) What is the cellular source of ADAM10 and is it localized to synapses (Aim 1)? 2) Do other subcortical synapses within the barrel circuit remodel via ADAM10-CX3CL1-CX3CR1 signaling and does this differ between whisker lesioning and trimming (Aim 2)? I hypothesize ADAM10 is derived from layer IV excitatory neurons to regulate microglia- mediated synapse remodeling and that ADAM10 signaling is specific for cortical synapse rewiring after whisker trimming and lesioning, but not for sub-cortical synapse remodeling. To test this hypothesis, I have acquired powerful in vivo molecular genetic tools to manipulate ADAM10 function in specific cells. I have also developed collaborations to learn and perform cutting-edge whole tissue clearing by iDISCO to assess structural remodeling of entire circuits. Finally, I have a strong mentoring team that includes my mentor Dr. Dorothy Schafer with expertise in microglial function within neural circuits, my co-mentor Dr. Andrew Tapper with expertise in structural and functional mapping of brain circuits, and collaborators with expertise in iDISCO. Together, I am in a strong position to molecularly dissect how ADAM10 modulates neuron-microglia signaling necessary for remodeling brain circuits. This could be highly relevant for neurodegenerative disease where microglial dysfunction, synapse loss, and ADAM10 have been implicated. In the process, I will receive training in a variety of microscopy and molecular genetic approaches that will provide a foundation for my future career as an independent principle investigator at an academic institution focused on dissecting functions for glial cells within neural circuits.

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EXTERNAL AWARDS FOR RESEARCH TRAINING (PAST)

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    Gq Receptor Regulation of Striatal Dopamine Transporters

    Dopamine (DA) neurotransmission is vital for behaviors such as movement and reward, as well as, cognitive functions including mood, learning and memory. Several neuropsychiatric disorders are linked to alterations in DA signaling including Attention Deficit Hyperactivity Disorder (ADHD), schizophrenia, Parkinson's disease, and addiction. The DA transporter (DAT) is imperative for temporal and spatial control of DA signaling. DAT is located at the presynaptic terminal of DAergic neurons and facilitates the termination of DAergic transmission by rapidly clearing released DA. DAT is the primary target of addictive and therapeutic psychostimulants, which compete for DA binding and block uptake through the transporter, preventing DA clearance and leading to the hyper-locomotive and rewarding behaviors associated with drug use. Given that DAergic signaling is highly sensitive to DAT function, understanding the molecular mechanisms that control DAT function and availability is a critical missing piece of the puzzle in understanding DAergic neurotransmission and dysfunction in DA- related disorders. Over two decades of research support that DAT surface expression is acutely regulated by endocytic trafficking. Protein kinase C (PKC) activation with phorbol esters stimulates DAT internalization and thereby decreases DAT surface expression and function. Although considerable progress has been made to define the molecular mechanisms governing basal and PKC-regulated DAT trafficking, there are significant gaps in our understanding of this process in bona fide DAergic terminals. It is not clear how DAT is regulated in response to the endogenous presynaptic receptors that are activated upstream of PKC, such as Gq-coupled receptors, and how the complex signal events stemming from Gq receptor activation integrate to acutely control DAT surface expression. It is additionally unknown whether regulated DAT trafficking is region-specific, or whether altered DAT surface expression impacts DAergic signaling in the striatum. The proposed studies will leverage chemogenetic receptors to test how Gq activation impacts DAT surface levels in a cell- autonomous manner, in both dorsal and ventral striatum. We will capitalize on a novel conditional, inducible, in vivo gene silencing approach to determine the endocytic mechanisms that are required for Gq-mediated DAT trafficking, by both chemogenetic and endogenous presynaptic receptors. We will further employ ex vivo fast- scan cyclic voltammetry to investigate how presynaptic DAT trafficking impacts DA signaling. I anticipate that at the completion of these studies, we will have gained a more in-depth understanding of the complex mechanisms underlying DAT regulation at presynaptic DAergic terminals, and its potential influence on synaptic DA homeostasis.

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    Fluorescent visualization of complement-dependent pannexin activity in microglia

    The goal of this project is fluorescently visualize ATP release and extracellular accumulation at the surface of stimulated microglia. The development of this innovative technology has the potential to enable spatiotemporal imaging of microglial extracellular signaling. For this project, I am exploiting the presence of the cell's glycocalyx to attach ATP-sensitive biosensors at the sites of ATP accumulation. There are two aims to this project: 1) to synthesize a novel, polyhistidine binding moiety that covalently modifies the glycocalyces of living cells and binds recombinant biosensors to measure ion and metabolite efflux and accumulation; 2) to visualize and measure ATP release from pannexin channels in C5a stimulated microglia. The completion of these aims will yield a transformative set of chemical-biological tools and methodologies to investigate the physiology and pathophysiology of pannexin-dependent activity in glia, and potentially in living animals.

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