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Conference National Academy of Sciences Colloquium on the Neurobiology of Pain (1998 : Irvine, Calif.) http://id.loc.gov/authorities/names/no2004004297
Title Papers from a National Academy of Sciences Colloquium on the Neurobiology of Pain / [organized by John Liebeskind, Ronald Dubner and Michael Gold].
Imprint Washington, D.C. : National Academy of Sciences, [1999]

Conference National Academy of Sciences Colloquium on the Neurobiology of Pain (1998 : Irvine, Calif.) http://id.loc.gov/authorities/names/no2004004297
Series National Academy of Sciences colloquium series.
National Academy of Sciences colloquium series. http://id.loc.gov/authorities/names/n99009085
Subject Neurobiology -- Congresses.
Nociceptors -- Congresses.
Pain perception -- Congresses.
Sodium channels -- Congresses.
Ion channels -- Congresses.
Alt Name Liebeskind, John C.
Dubner, Ronald.
Gold, Michael Robert.
National Academy of Sciences (U.S.)
Alternate Title Proceedings of the National Academy of Sciences of the United States of America.
Colloquium on the Neurobiology of Pain.
Colloquium on Neurobiology of Pain.
Add Title Neurobiology of pain
Description 1 online resource (pages 7627-7755) : illustrations.
polychrome rdacc http://rdaregistry.info/termList/RDAColourContent/1003
Note " ... papers, which were presented at the National Academy of Sciences colloquium "The Neurobiology of Pain," held December 11-13, 1998, at the Arnold and Mabel Beckman Center in Irvine, CA"--Page 7627.
"July 1999"--Page 7627.
Bibliography Note Includes bibliographical references.
Note Print version record.
Contents COLLOQUIUM ON NEUROBIOLOGY OF PAIN -- NATIONAL ACADEMY OF SCIENCES Colloquium Series -- List of Attendees -- Contents -- The neurobiology of pain -- John C. Liebeskind (1935a?1997): A tribute -- Sodium channels and pain -- HYPEREXCITABILITY IN DRG CELLS AFTER INJURY -- MULTIPLE SODIUM CHANNELS IN PRIMARY SENSORY NEURONS -- SODIUM CHANNEL GENE EXPRESSION IS ALTERED AFTER INJURY TO DRG NEURONS -- PHYSIOLOGIC CHANGES ACCOMPANY ALTERED SODIUM GENE EXPRESSION AFTER DRG NEURON INJURY -- NEUROTROPHINS MODULATE SODIUM CHANNEL EXPRESSION IN DRG NEURONS
SODIUM CHANNEL EXPRESSION IN INFLAMMATORY PAIN MODELSSODIUM CHANNELS AS MOLECULAR TARGETS IN PAIN RESEARCH -- A comparison of the potential role of the tetrodotoxin-insensitive sodium channels, PN3/SNS and NaN/SNS2, in rat models of ... -- EVIDENCE FOR A ROLE FOR PN3 IN THE MEDIATION OF ABNORMAL PAIN BEHAVIORS AFTER NERVE AND TISSUE INJURY -- THE PATHOPHYSIOLOGICAL CONTRIBUTION OF NAN/SNS2 IN PERIPHERAL NERVE INJURY? -- CONCLUSIONS -- Tetrodotoxin-resistant Na+ currents and inflammatory hyperalgesia -- WHY FOCUS ON NA+ CHANNELS? -- WHY TTX-RESISTANT CHANNELS?
CONCLUSIONSCalcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons -- RESULTS -- DISCUSSION -- Ion channels gated by heat -- Causalgia, pathological pain, and adrenergic receptors -- Forebrain mechanisms of nociception and pain: Analysis through imaging -- A visceral pain pathway in the dorsal column of the spinal cord -- ASCENDING PATHWAYS THAT MEDIATE VISCERAL NOCICEPTIVE TRANSMISSION -- MORPHOLOGICAL STUDIES OF THE VISCERAL POSTSYNAPTIC DC SYSTEM -- BEHAVIORAL EVIDENCE FOR A DC VISCERAL PAIN PATHWAY
FUNCTIONAL MRI STUDIES IN MONKEYSThe spinal biology in humans and animals of pain states generated by persistent small afferent input -- BEHAVIORAL EFFECTS OF CUTANEOUS STIMULI AFTER INJURY -- ROLE OF SPINAL AND PERIPHERAL SYSTEMS IN THE POST-TISSUE INJURY PAIN STATE -- CHARACTERIZATION OF SEVERAL SPINAL COMPONENTS LEADING TO POSTINJURY PAIN STATES -- Spinal Pharmacology of Facilitated Processing -- SYSTEM INTERACTIONS -- HUMAN SPINAL PROCESSING -- Supraspinal contributions to hyperalgesia -- Neurotrophins and hyperalgesia -- CONCLUSIONS
Src, a molecular switch governing gain control of synaptic transmission mediated by N-methyl-D-aspartate receptorsCONCLUSIONS -- Pain perception: Is there a role for primary somatosensory cortex? -- Implications of immune-to-brain communication for sickness and pain -- IMMUNE-TO-BRAIN COMMUNICATION IN SICKNESS -- PAIN AS A NATURAL OUTCOME OF IMMUNE-TO-BRAIN COMMUNICATION -- Role of Spinal Cord Glia in Exaggerated Pain -- CONCLUSIONS AND IMPLICATIONS -- Brain-derived neurotrophic factor is an endogenous modulator of nociceptive responses in the spinal cord
ISBN 0309569338 (electronic bk.)
9780309569330 (electronic bk.)
OCLC # 57735171
Additional Format Print version: National Academy of Sciences Colloquium on the Neurobiology of Pain (1998 : Irvine, Calif.). Papers from a National Academy of Sciences Colloquium on the Neurobiology of Pain. Washington, D.C. : National Academy of Sciences, [1999] (OCoLC)54038127.