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Understanding Somatosensation and Pain: The 2013 Dr. Paul Janssen Award Symposium

Understanding Somatosensation and Pain: The 2013 Dr. Paul Janssen Award Symposium

Thursday, September 19, 2013

The New York Public Library, South Court Auditorium

Presented By

Presented by the Dr. Paul Janssen Award for Biomedical Research and the New York Academy of Sciences


The scientific breakthroughs of Dr. David Julius, PhD, have greatly advanced our knowledge of the molecular mechanisms of touch, pain, and thermosensation. His research has led to an understanding of pain hypersensitivity, and how neurons sense stimuli and transmit signals to the brain. In 1997, Dr. Julius published a groundbreaking study in which his group identified and cloned the transient receptor potential (TRPV1) ion channel based on its activation by capsaicin from chili peppers as well as by excessive heat, explaining the burning hot sensation caused by skin contact with capsaicin. Dr. Julius identified additional ion channels on sensory nerves using other natural agents, including menthol from mint leaves and tarantula toxins, as pharmacological probes. In recognition for his role in discovering a unifying mechanism for nociception and thermosensation, Dr. Julius will receive the 2013 Dr. Paul Janssen Award for Biomedical Research.

This symposium will honor Dr. Julius, who will reflect on his early discoveries and ongoing research to better understand thermosensation and how this mechanism contributes to the perception of acute, chronic, and inflammatory pain. Following the Award lecture, leading scientists in the somatosensory field will discuss new insights on the biology of pain and translational research that may lead to new therapies for chronic pain and inflammatory syndromes.


David Julius, PhD

University of California, San Francisco

Registration Pricing

Symposium registration is free. Although on-site registration may be possible on the day of the event, pre-registration is highly encouraged due to space limitations.

This symposium is made possible with support from


* Presentation titles and times are subject to change.

September 19, 2013

8:00 AM

Registration and Breakfast

9:00 AM

Welcome and Introductory Remarks
Seema Kumar, Johnson & Johnson
Brooke Grindlinger, PhD, The New York Academy of Sciences

SESSION I: Identifying the Mechanisms of Pain Signaling

9:15 AM

2013 Dr. Paul Janssen Award for Biomedical Research Announcement
William N. Hait, MD, PhD, Janssen R&D

9:30 AM

2013 Dr. Paul Janssen Award for Biomedical Research Lecture
Our Understanding of Somatosensation and Pain
David Julius, PhD, University of California, San Francisco

SESSION II: Understanding the Biological Mechanisms of Pain and How to Treat It

10:10 AM

Session Introduction:

New Developments in Pain Treatment
Husseini Manji, MD, FRCPC, Janssen R&D

10:20 AM

Transplant Therapies for Chronic Neuropathic Pain
Allan I. Basbaum, PhD, FRS, University of California, San Francisco

10:45 AM

Understanding the Neural Basis of Pain Processing
M. Catherine Bushnell, PhD, National Institutes of Health

11:10 AM

Developing Novel Analgesics to Target the Pain Pathway
Clifford Woolf, MB, BCh, PhD, Children's Hospital Boston, Harvard University

11:35 AM

Panel Discussion: Perspectives on Translating Pain Research From Bench to Bedside


David S. Bredt, MD, PhD, Janssen R&D

David Julius, PhD, University of California, San Francisco
Allan I. Basbaum, PhD, FRS, University of California, San Francisco
M. Catherine Bushnell, PhD, National Institutes of Health (NIH)
Clifford Woolf, MB, BCh, PhD, Children's Hospital Boston, Harvard University

12:00 PM

Closing Remarks
Seema Kumar, Johnson & Johnson

12:05 PM


1:30 PM




David Julius, PhD

University of California, San Francisco

David Julius was born in Brighton Beach, Brooklyn, where he attended public elementary and high schools. He received his undergraduate degree from MIT, gaining his first research experience in the laboratory of Alexander Rich studying mechanisms of tRNA aminoacylation. David then moved to UC Berkeley for graduate studies, where he worked with Jeremy Thorner and Randy Schekman to elucidate mechanisms of peptide hormone processing and secretion in Saccharomyces yeast, culminating in the identification of KEX2 as the founding member of a family of prohormone convertases required for proteolytic maturation of insulin, endorphins, and many other peptide hormones. For postdoctoral studies, David joined Richard Axel's group at Columbia University, where his focus turned to neuropharmacology and receptor function. During this time, David developed powerful expression cloning methods that helped revolutionize molecular pharmacology while enabling him to identify genes encoding members of the serotonin receptor family. He then joined the faculty at UC San Francisco, where he is currently Professor and Chair of Physiology. David's research is focused on understanding the molecular basis of pain sensation.


Allan I. Basbaum, PhD, FRS

University of California, San Francisco

Allan I. Basbaum, PhD, FRS is Professor and Chairman of the Department of Anatomy at the University of California, San Francisco. Dr. Basbaum's interest in pain research began with Ronald Melzack at McGill University. After receiving a PhD from the University of Pennsylvania, he did postdoctoral research at University College London, with Patrick Wall. He moved to UC San Francisco and was appointed to the faculty in 1977. Dr. Basbaum's research concerns the molecular mechanisms that underlie the development of persistent pain after tissue or nerve injury. He has served on the council and as Treasurer of the International Association for the Study of Pain, and in January 2013 relinquished his position as editor-in-chief of Pain. Dr. Basbaum has been a Board Member and Program Chair of the American Pain Society (APS). He is a recipient of the F. W. L. Kerr Memorial Award from the APS and the Bristol-Myers Squibb Prize for Distinguished Pain Research. He was elected to the American Academy of Arts and Sciences, to the Institute of Medicine and the British Academy of Medical Science. He is also a Fellow of the American Association for the Advancement of Science and of the Royal Society in the UK.

David S. Bredt, MD, PhD

Janssen R&D

In March 2011, Bredt was hired by Johnson & Johnson Pharmaceutical Group as Global Head of Neuroscience Discovery. In this role he oversees preclinical biology and chemistry research. He is also in charge of clinical and preclinical biomarker and pharmacogenomics programs that support Johnson & Johnson's neuroscience franchise. His previous industry experience was with Eli Lilly and Company (2004–2011) where he was Vice President of Integrative Biology and Vice President of Neuroscience Research.

Bredt graduated summa cum laude in Chemistry at Princeton University in May 1986. He received his MD and PhD at Johns Hopkins University School of Medicine (1993), where he trained with Dr. Solomon H. Snyder. Prior to joining Lilly, Bredt was Professor of Physiology at the University of California, San Francisco. His research on nitric oxide, glutamate receptor signaling, and synaptic plasticity has yielded more than 200 papers, which have been cited over 38,000 times in the scientific literature. He served on the Medical Advisory Committee for the Muscular Dystrophy Association, he was an Established Investigator for the American Heart and he was a Presidential Young Investigator for the National Science Foundation.

M. Catherine Bushnell, PhD

National Institutes of Health

M. Catherine Bushnell, PhD is Scientific Director of the National Center for Complementary and Alternative Medicine (NCCAM) at the NIH, where she is responsible for establishing and overseeing a new program on the brain's role in perceiving, modifying, and managing pain. Prior to her appointment at NCCAM, Dr. Bushnell was the Harold Griffith Professor of Anesthesia at McGill University, in Montreal, Canada. She has been president of the Canadian Pain Society, and Treasurer and Press Editor-in-Chief of the International Association for the Study of Pain. Among her other honors are the Lifetime Achievement Award from the Canadian Pain Society and the Frederick Kerr Basic Science Research Award from the American Pain Society. Dr. Bushnell holds a PhD in Experimental Psychology from the American University, Washington, DC and received postdoctoral training in Neurophysiology at the NIH. Her research interests include forebrain mechanisms of pain processing, psychological modulation of pain, and neural alternations in chronic pain patients. Recent projects have utilized brain imaging and psychophysical testing to study the neural basis of pain processing, addressing both normal pain processing and aberrant processing after nervous system damage.

Husseini Manji, MD, FRCPC

Janssen R&D

Husseini K. Manji, MD, FRCPC, is Global Therapeutic Head for Neuroscience at Janssen Research & Development, LLC, a division of Johnson & Johnson. Previously, he was Chief, Laboratory of Molecular Pathophysiology & Experimental Therapeutics, NIH, and Director of the NIH Mood and Anxiety Disorders Program. Dr. Manji received his BS and MD from the University of British Columbia. He completed fellowship training at the NIMH and completed additional training in cellular and molecular biology. His research has focused on investigation of disease-and treatment-induced changes in gene and protein networks that regulate synaptic and neural plasticity. His work has led to investigation of novel therapeutics for patients with refractory neuropsychiatric illnesses. Dr. Manji has also been involved in medical and postgraduate neuroscience education and has published extensively on the molecular and cellular neurobiology of neuropsychiatric disorders and the development of novel therapeutics. Dr. Manji has received numerous distinguished scientific and academic awards, including the NIMH Director's Career Award for Significant Scientific Achievement, and was inducted in to the US Institute of Medicine of the National Academies in 2008. He has served as Chair of the American College of Neuropsychopharmacology, is a Counselor to the Society of Biological Psychiatry, and serves on a variety of editorial boards of scholarly journals. He holds voluntary leadership positions in many organizations devoted to advancement of neuroscience and advocacy for people with neuropsychiatric illnesses. He has been a member of the Howard Hughes Medical Institute and NIH Research Scholars Program Advisory Committee.

Clifford Woolf, MB, BCh, PhD

Boston Children's Hospital, Harvard University

Clifford Woolf, MB, BCh, PhD [University of Witwatersrand, Johannesburg, South Africa] is Director of the F. M. Kirby Neurobiology Center and the Program in Neurobiology at Boston Children's Hospital in Massachusetts, a Professor of Neurology and Neurobiology at Harvard Medical School, and a faculty member of the Harvard Stem Cell Institute. His pain research focuses on understanding basic mechanisms and translating the results into new therapeutics and diagnostics. He discovered central sensitization and showed that nerve growth factor plays a role in inflammatory pain. His current work includes human, mouse, and Drosophila genetics, stem cell biology, and a strategy for silencing pain fibers to relieve pain. Dr. Woolf is also a serial innovator, holding 15 patents, patent applications, and licenses for technological innovations in pain management; and he serves as a Consultant and Advisory Board Member for several biotechnology firms and drug companies. Recently, he received a Javits Award from the National Institute of Neurological Disorders and Stroke of the US National Institutes of Health, and delivered the Bonica Lecture for the International Association for the Study of Pain. Dr. Woolf is a dedicated teacher and mentor and has served on many national and international committees on pain research and treatment.


This symposium is made possible with support from

  • Janssen Award
  • Johnson & Johnson

Promotional Partners

New York Academy of Medicine

Scientific American

New York State Pain Society


Session I: Identifying the Mechanisms of Pain Signaling

Our Understanding of Somatosensation and Pain
David Julius, PhD, University of California, San Francisco

We are interested in determining the molecular basis of somatosensation—the process whereby we experience touch and temperature—with an emphasis on identifying molecules that detect noxious (pain-producing) stimuli. We are also interested in understanding how somatosensation is altered in response to tissue or nerve injury. Our approach has been to identify molecular targets for natural products that mimic the psychophysical effects of commonly encountered somatosensory stimuli, such as heat or cold, and to then ask how these molecules are activated or modulated by noxious stimuli or injury.
We have focused on three members of the TRP channel family (TRPV1, TRPM8, and TRPA1) that are expressed by subpopulations of primary afferent sensory neurons and which have been implicated in the detection of thermal stimuli and/or inflammatory agents. Genetic studies support the idea that the capsaicin receptor (TRPV1) and the menthol receptor (TRPM8) function as detectors of heat and cold, respectively, whereas the wasabi receptor (TRPA1) functions as a detector of environmental and endogenous chemical irritants.
From a signal transduction and therapeutics perspective, there is great interest in understanding how these channels are activated (gated) by physical and/or chemical stimuli. We have used a combination of unbiased genetic screening and natural product biochemistry to address these issues and probe mechanisms of stimulus detection, channel activation, and coding logic of the somatosensory system.

Session II: Understanding the Biological Mechanisms of Pain and How to Treat It

Transgenic Mice as a Tool to Study Pain and its Control
Allan Basbaum, PhD, FRS, University of California, San Francisco

The "pain pathway" traditionally includes nociceptors (i.e. pain-fibers), their connections with dorsal horn projection neurons that transmit pain messages to the brain, and the brain networks that generate the pain percept. This simple view ignores the dorsal horn circuits that regulate the output of the projection neuron. Because of the great interest in understanding the pathophysiological changes that underlie injury-induced chronic pain conditions, most attention has been paid to the inhibitory interneurons that populate the dorsal horn and that regulate the output of the projection neurons. Indeed, loss of function of these inhibitory interneurons is presumed to contribute to the spontaneous pain and hypersensitivity that characterizes many chronic pain conditions. With a view to overcoming more directly nerve injury-induced loss of these inhibitory controls, we have recently reported that transplants of embryonic cortical GABAergic precursor cells into the adult spinal cord can dramatically reduce the mechanical and thermal hypersensitivity produced by both traumatic and chemotherapy-induced peripheral nerve injury. Transgenic studies also emphasize the contribution of the excitatory interneurons. For example, our laboratory described results obtained in a mouse in which the TR4 orphan nuclear receptor was deleted in neurons. These mice have a profound loss of behaviors indicative of pain and itch. This phenotype results from a loss of a large population of superficial dorsal horn excitatory interneurons. It follows that pharmaceuticals directed selectively at the circuits engaged by these excitatory interneurons will have beneficial therapeutic effects, which could supplement the gains obtained from treatments directed at enhancing inhibitory controls.

Understanding the Neural Basis of Pain Processing
M. Catherine Bushnell, PhD, National Institutes of Health

Brain imaging reveals that multiple regions of the brain are activated during pain, including the thalamus, somatosensory cortices, and limbic regions, such as anterior cingulate and insular cortices. Frontal cortical regions and periaqueducal grey matter are involved in pain modulation, and become particularly important in chronic pain conditions. Functional brain imaging studies of touch-evoked allodynia in patients with chronic pain reveal that similar brain regions are activated. Whether the pain is related to peripheral nerve damage or damage within the CNS, there is an abnormal activation of pain-related regions by stimuli that normally would not be painful. Resting-state imaging studies of spontaneous pain related to nerve injury also reveal a network of brain activation and a disruption of normal resting-state brain activity. There is now accumulating evidence that chronic pain is associated with changes in brain anatomy. Decreased volume of brain gray matter has been described for a variety of pain syndromes. The decreases in gray matter are related to duration and intensity of symptoms, suggesting that the structural changes may be an important component of the chronification of pain. A longitudinal imaging study in a rodent neuropathic pain model reveals a similar decrease in gray matter of the frontal cortex related to the intensity of tactile allodynia. However, the gray matter decreases only begin months after the onset of pain and are temporally associated with the onset of anxiety-like behavior, suggesting that such deceases could be related to the emotional consequences of long-term pain. Together, brain imaging studies suggest that chronic pain conditions can have a profound influence on the brain that may then lead to secondary conditions, including anxiety disorders and depression. As such, the data underline the important of early treatment of chronic pain conditions.

Developing Novel Analgesics to Target the Pain Pathway
Clifford Woolf, MB, BCh, PhD, Boston Children's Hospital, Harvard University

Infection with Staph aureus produces marked pain that at least in the acute phase is quite independent of activation of the immune system and involves at least two contributing mechanisms; the first involves heat stable formyl peptides produced by the bacteria and which act on the FPR-1G-protein coupled receptor expressed by nociceptors to produce a TRPA1 coupled activation of the sensory neurons (Chiu et al, 2013). The second results from secretion by the bacteria of a pore forming toxin, alpha hemolysin. This large protein punches a hole selectively in the membrane of TRPV1 expressing nociceptors by an ADAM10 binding mechanism to produce direct activation of the sensory fibers. Essentially the pathogen provides a non-selective ion channel to the neuron to activate it, resulting in the detection by the nervous system of the presence of the pathogen by the production of pain. These insights provide new opportunities to reduce the pain of bacterial infections.

Travel & Lodging

Event Location

New York Public Library, South Court Auditorium
Stephen A. Schwarzman Building
5th Avenue at East 42nd Street
New York, NY 10018

Directions to the New York Public Library

Hotels near the New York Public Library

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The Rockefeller Center location is a 12 minute walk away from the event location.

Other area hotels
Library Hotel 212.983.4500
Hotel Giraffe New York 212.685.7700
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