May 18, 2015 - Yang Xiang, Ph.D., awarded NIH grant: Molecular Mechanisms of nociceptor sensitization
Inflammatory pain, characterized by enhanced pain sensation after tissue injury, is one of the major types of pain hypersensitivity, and may cause chronic pain when not treated properly. However, the cellular and molecular mechanisms of inflammatory pain is not well understood. It was recently found that tissue injury induces inflammatory pain in fruit fly Drosophila, a classical genetically tractable model organism. Importantly, mechanisms of inflammatory pain is highly conserved between fruit flies and humans, arguing that studies in fruit flies can offer novel insights into pain hypersensitivity in humans. In the current proposal, we propose to study pain hypersensitivity at single cell resolution in Drosophila larvae, focusing on how tissue injury enhances excitability of nociceptive sensory neurons.
May 8, 2015 - Michael Francis, Ph.D., awarded NIH grant: Neuromodulator signaling and context dependent behavior
This proposal aims to understand how medically relevant neuromodulatory signaling, initiated by the conserved NLP-12/cholecystokinin (CCK) neuropeptide, shapes neural circuit activity and context-dependent behavior. Alterations in neuropeptide signaling, and in particular CCK signaling, are linked with a wide variety of neuropsychiatric conditions, including panic and anxiety disorders as well as schizophrenia; yet it is too difficult to understand the pathophysiology of these diseases because our understanding of how neuromodulatory systems shape neural activity remains inadequate. By studying a conserved neuromodulatory system in the simple model organism C. elegans, we expect to obtain a new level of understanding of how neuromodulators shape circuit activity, ultimately leading to the development of new therapies for brain disorders.
March 2, 2015 - Michael Francis, Ph.D., awarded NIH grant: Molecluar analysis of neural circuit excitation and inhibition
The neurotransmitter acetylcholine plays conserved roles in mediating communication between neurons from nematodes to humans. Alterations in acetylcholine-mediated signaling are a hallmark of a wide variety of degenerative neurological disorders and nicotine addiction, yet we know very little about the molecular pathways that regulate this process in the mature nervous system or about how deficits alter connectivity in the developing nervous system. Our work will provide fundamental knowledge about mechanisms for regulation of acetylcholine-mediated signaling and is expected to provide critical insights into how defects in acetylcholine-mediated signaling cause disease.
January 30, 2015 - Alison Philbrook, of Dr. Michael Francis' Lab, awarded the National Reserach Service Award Fellowship: Molecular regulation of nicotinic acetylcholine receptors
Smoking-related diseases result in more than 400,000 premature deaths in the United States each year, yet thousands struggle with smoking cessation. Nicotine, the major addictive component in tobacco, interacts with specific classes of nicotine acetylcholine receptors (nAChRs), altering the functional state of the receptors and expression at the cell surface. Although the role of nAChRs in nictoine addiction has been well established, mechanisms for the biological regulation of these receptors during normal brain function and following nicotine exposure are poorly defined. This proposal aims to understand the dynamics nAChRs on the neuronal cell surface using the model system C. elegans. Given the high degree of evolutionary conservation between nematodes and mammals, it is expected that the findings will be directly relevant for understanding the biology of nAChRs in the mammalian brain.
January 1, 2015 - Jaeda Coutinho-Budd, of Dr. Marc Freeman's Lab, awarded the American Cancer Society Postdoctoral Fellowship: Cellular and Molecular Mechanisms Regulating Glial Growth Control
Local and regional spread of tumors is driven by increased cell invasiveness and metastasis, whereby primary tumors spread to secondary tissues. Precisely how tumor cells become invasive is poorly understood, but understanding this transformation remains a major goal in basic biomedical research. Glioma, a tumor that generates in the nervous system, broadly describes a category of molecularly heterogeneous tumors that typically arise from glial cells such as astrocytes or oligodendrocytes. Not only are many high-grade gliomas often resistant to chemotherapy, but their invasive nature makes surgical removal nearly impossible. Prior to tumorigenesis, glia play important roles in regulating nervous system function, such as providing trophic factors for neurite growth and guidance, and facilitating synapse formation and maturation. However, genetic lesions transform these beneficial cells into destructive cancers through a variety of unidentified mechanisms. It is therefore paramount to better understand the basic molecular and genetic mechanisms that regulate glial proliferation, growth and infiltration. The goal of this project is to use Drosophila melanogaster to determine how these processes go awry in glial disease.
October 6, 2014 - Carlos Lois, M.D., Ph.D., awarded a collaborative BRAIN Initiative grant with Stanford University, Brandeis University and Cold Spring Harbor Laboratory: Combining genetics, genomics, and anatomy to classify cell types across mammals
Most of what is known about how neurons work is based on experiments that have been done in mice or rats. We know that human brains are more complex that mice or rat brains, but we really do not understand exactly how evolution has progressed from the rodent to the human brain. We will compare the properties and function of identical neurons genetically identified in in transgenic mice and rats to find out in which properties they differ. We will also examine which genes are different (in those genetically identified neurons) between mice and rats so that we could explain how the differences in gene expression account for the differences in function. This kind of information will allow us to understand the logic of evolution by which neurons become more complex from lower animals to higher animals, and eventually, to understand why the human brain can do things that no other animal brain can do.
The Department of Neurobiology would like to welcome our newest faculty member, Assistant Professor, Dorothy "Dori" Schafer, Ph.D! Dr. Schafer will join us on January 1, 2015
Budnik named fellow of the Hedwig van Ameringen Executive Leadership in Academic Medicine (ELAM)
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Congratulations on our 2014 Faculty Promotions:
June 19, 2014 - Marc Freeman, Ph.D., promoted to Professor
May 16, 2014 - Patrick Emery, Ph.D., promoted to Professor and Mark Alkema, Ph.D. promoted to Associate Professor
March 21, 2014 - Michael Francis, Ph.D., promoted to Associate Professor
Budnik receives prestigious MERIT award from NIH
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Report on monarch butterfly dropoff cites work by Steve Reppert at UMMS
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Budnik gets EUREKA grant to study communication between nucleus and cytoplasm
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Marc R. Freeman, PhD, named Howard Hughes Medical Institute investigator