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The Gill Center for Biomolecular Science

Gill Seminars

Previous Speakers

Upcoming Speakers

September 22, 2017
Wei Wei, Ph.D.

The University of Chicago

Seminar will be held in Multidisciplinary Science Building II (MSBII), Room 102 at 12:00 p.m.

Title: Neural mechanisms of motion detection in the mammalian retina

Abstract: A critical function of neural circuitry in the brain is detecting relevant features in the environment. The direction selective circuit in the retina is an excellent model system to study feature detection at the cellular and synaptic levels. In this talk, I will discuss our recent work that focuses on the dendritic and synaptic mechanisms underlying direction selectivity using a combination of synapse-specific genetic manipulations, two-photon calcium imaging, electrophysiology and pharmacology. Our results demonstrate that dynamic and multilayered synaptic mechanisms are recruited to encode motion direction under different visual conditions, and highlight the importance of using both simple and complex stimuli that reflect the challenges posed by the natural environment during circuit interrogation.

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September 27, 2017
Clifford J. Woolf, M.B., B.Ch., Ph.D.

FM Kirby Neurobiology Center and Program in Neurobiology
Boston Children's Hospital
Harvard Medical School

Seminar will take place in the Indiana Memorial Union, Whittenberger Auditorium
during the 2017 Gill Symposium

Title: Unravelling pain one millisecond at a time

Abstract: Pain is initiated by the activation of high threshold sensory neurons; the nociceptors – which serve to detect danger. We are using stem cell technology, live nociceptor imaging in the whole animal, optogenetics and automated behavior analysis to tease out what behaviors are elicited by these danger detectors. This turns out to be a repertoire of complex, widespread, context-dependent subsecond behaviors which reveal new insight into how the nervous system operates at the cell, circuit and system level.

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September 27, 2017
Diana Bautista, Ph.D.

University of California, Berkeley

Seminar will take place in the Indiana Memorial Union, Whittenberger Auditorium
during the 2017 Gill Symposium

Title: Neural control of chronic itch and inflammation in atopic disease

Abstract: Chronic itch is a highly prevalent and debilitating disorder with few effective treatments. The most common chronic itch disorder is atopic dermatitis (eczema), an inflammatory skin condition affecting 10-20% of people worldwide. In a process termed the atopic march, atopic dermatitis is often followed by the onset of additional atopic diseases, including allergic rhinitis, asthma and allergy. Atopic disease is thought to arise from loss of skin barrier integrity and dysregulated immune cell activity. Our recent studies show that the peripheral nervous system also plays a key role in atopic disease pathogenesis. I will discuss our recent studies highlighting the molecular crosstalk between epithelial cells, immune cells and peripheral somatosensory neurons that promote chronic itch and inflammation.

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September 27, 2017
Xinzhong Dong, Ph.D.

Johns Hopkins University School of Medicine

Seminar will take place in the Indiana Memorial Union, Whittenberger Auditorium
during the 2017 Gill Symposium

Title: The mechanisms of itch and inflammation

Abstract: Despite of the clinical importance, cell surface receptors mediating non-histaminergic itch are largely unknown. We identified a large family of G protein-coupled receptors in mice called Mrgprs. Many of these receptors are exclusively expressed in distinct subsets of small-diameter dorsal root ganglion (DRG) neurons. We found that MrgprA3 functions as a receptor for chloroquine (an anti-malaria drug) and is required for chloroquine-induced itch. Besides chloroquine, Mrgprs also respond to several itch-inducing compounds such as BAM8-22, SLIGRL, and beta-alanine suggesting that Mrgprs are novel itch receptors by directly sensing these compounds. Our data have shown the involvement of Mrgprs in mouse chronic itch models such as dry skin, contact dermatitis, and allergic itch. Importantly, some of the results have been confirmed in human psychophysical studies. In addition, we demonstrated for the first time that itch-specific sensory neurons do exist and are distinct from pain-sensing neurons. Besides the sensory neuron specific Mrgprs, we discovered another member of the gene family, MrgprB2, is exclusively expressed in mast cells, a type of innate immune cells, which secret many pro-inflammatory mediators like histamine upon activation. We found that human MrgprX2 and mouse MrgprB2 are the sole receptor of many basic secretagogues mediating IgE-independent mast cell activation and responsible for many drug-induced pseudo-allergic side effects. Therefore, we believe that targeting human Mrgprs may lead to novel treatment of various diseases in the future. ​

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September 27, 2017
Michael W. Salter, M.D., Ph.D., FRSCC
Hospital for Sick Children (Sick Kids) and University of Toronto

Seminar will take place in the Indiana Memorial Union, Whittenberger Auditorium
during the 2017 Gill Symposium

Title: Sex, pain and microglia

Abstract: Neuron-microglial interactions are increasingly recognized as being key for physiological and pathological processes in the central nervous system.  Microglia have been found to play a causal role in neuropathic pain behaviours resulting from peripheral nerve injury, and a core neuron-microglia-neuron signaling pathway has been elucidated. Within the dorsal horn, microglia suppress neuronal inhibition by a cascade involving activation of microglial P2X4 receptors causing the release of brain derived neurotrophic factor (BDNF).  BDNF acts on trkB receptors which leads to a rise in intracellular Cl- concentration in dorsal horn nociceptive output neurons, transforming the response properties of these neurons.   In addition to suppressing inhibition, peripheral nerve injury causes activity-dependent potentiation at dorsal horn glutamatergic synapses which enhances nociceptive transmission. BDNF mediates the enhancement of synaptic NMDAR responses through activation of TrkB and the Src-family kinase, Fyn. We have discovered that microglia-to-neuron signaling is not only critical for pain hypersensitivity after nerve injury but also for the paradoxical hyperalgesic effect of morphine and other opioids.  This core signaling pathway has been extensively characterized, in studies using male mice.  We have recently discovered that microglia-neuron signaling is dispensable in female mice.  Rather, pain hypersensitivity in female mice depends upon the adaptive immune system, likely upon T cells.  Despite this profound difference in cellular mechanisms, pain hypersensitivity in female mice is as robust as that in male mice.  Taking into consideration sex differences in the spinal immune-neuronal signaling has important implications ranging from diagnostics, to therapeutics, to prevention of chronic pain.
 
Funding: Supported by CIHR, Krembil Fdn, CRC, Anne and Max Tanenbaum Chairs, and Northbridge Chair.

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September 27, 2017
Wenqin Luo, Ph.D.

University of Pennsylvania

Seminar will take place in the Indiana Memorial Union, Whittenberger Auditorium
during the 2017 Gill Symposium

Title: Somatotopic Organization and Functions of Mammalian Non-peptidergic Nociceptors

Abstract: Despite a low density of pain-sensing neurites, the human distal limbs (i.e. hands and fingers) have a high sensitivity for noxious stimuli. This puzzling phenomenon cannot be explained by our current knowledge about the functional organization of the mammalian pain system. To answer this question, my lab systematically traced mouse nociceptor single-cell structure across the body using a newly generated non-peptidergic nociceptor specific MrgprDCreERT2 line. We found that, like humans, the mouse paw glabrous skin has a low density of MrgprD+ neurites compared to trunk skin. In addition, individual terminals in these locations are comparable in size. Surprisingly, the central terminals of paw and trunk innervating nociceptors have very distinct morphologies in the spinal cord, and development of these distinct central terminals occurs independently from their peripheral innervation. Consistent with this anatomical difference, plantar paw nociceptive circuits display a heightened signal transmission and lateral inhibition in spinal cord slice recordings and a reduced stimulus threshold for triggering nociceptive behaviors. Taken together, our results elucidate a novel somatotopic functional organization of the mammalian pain system that mainly employs central, rather than peripheral, mechanisms to generate a sensory fovea.  In addition, my lab recently developed a high speed imaging method for mouse paw withdraw reflex that allow us to objectively measure mouse pain status. Using this approach, we found that activation of MrgD+ non-peptidergic nociceptors, which were considered as a major type of pain-sensing neurons by the field, trigger pain in chronic inflammation but not baseline conditions.

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October 30, 2017
Benjamin Deneen, Ph.D.

Baylor College of Medicine

Seminar will be held in Psychology, Room 101 at 4:00 p.m.

Title: Developmental Gliogenesis: The Crossroads of Cell Fate and Malignancy in the CNS

Abstract: Astrocytes and oligodendrocytes comprise CNS glia and are the most abundant cell types in the adult brain, executing a vast array of physiological roles essential to brain function, including myelination, synapse formation, neurotransmission, and formation of the blood-brain barrier. Accordingly, glial cells directly contribute to a wide spectrum of neurological disorders, ranging from neurodevelopmental and degenerative, to injury and malignancy. 
            My laboratory seeks to unlock the mysterious and enigmatic biology surrounding glial cell development and function in the brain. Beginning with developmental gliogenesis, we identified  key transcriptional mechanisms controlling the initiation of gliogenesis in the embryonic CNS. Moving towards function, our recent endeavors focused on decoding the cellular and functional diversity of astrocytes in the adult brain. In both cases, we made fundamental observations about the nature of glial cells and directly applied these paradigms to relevant neurological diseases: brain tumors and white matter injury. Therefore my lecture will describe how we made these basic discoveries on the nature of glial cells and the approaches we used to apply these developmental paradigms to neurological disease.

Co-sponsored with Program in Neuroscience

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January 8, 2018
Alison Barth, Ph.D.

Carnegie Mellon University

Seminar will be held in Psychology, Room 101 at 4:00 p.m.

Title: Pending

Abstract: Pending

Co-sponsored with Program in Neuroscience

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February 26, 2018
Chiara Cirrelli, Ph.D.

University of Wisconsin-Madison

Seminar will be held in Psychology, Room 101 at 4:00 p.m.

Title: Pending

Abstract: Pending

Co-sponsored with Program in Neuroscience

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