Papers from a National Academy of Sciences Colloquium on the Neurobiology of Pain /

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Online Access: Full text (MCPHS users only)
Corporate Authors: National Academy of Sciences Colloquium on the Neurobiology of Pain Irvine, Calif., National Academy of Sciences (U.S.)
Other Authors: Liebeskind, John C., Dubner, Ronald, Gold, Michael Robert
Format: Electronic Conference Proceeding eBook
Language:English
Published: Washington, D.C. : National Academy of Sciences, 1999
Series:National Academy of Sciences colloquium series.
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Local Note:ProQuest Ebook Central

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111 2 |a National Academy of Sciences Colloquium on the Neurobiology of Pain  |d (1998 :  |c Irvine, Calif.) 
245 1 0 |a Papers from a National Academy of Sciences Colloquium on the Neurobiology of Pain /  |c [organized by John Liebeskind, Ronald Dubner and Michael Gold]. 
246 3 0 |a Neurobiology of pain 
260 |a Washington, D.C. :  |b National Academy of Sciences,  |c [1999] 
300 |a 1 online resource (pages 7627-7755) :  |b illustrations 
336 |a text  |b txt  |2 rdacontent 
337 |a computer  |b c  |2 rdamedia 
338 |a online resource  |b cr  |2 rdacarrier 
490 1 |a National Academy of Sciences colloquium series 
500 |a " ... 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. 
500 |a "July 1999"--Page 7627. 
504 |a Includes bibliographical references. 
505 0 |a COLLOQUIUM ON NEUROBIOLOGY OF PAIN -- NATIONAL ACADEMY OF SCIENCES Colloquium Series -- List of Attendees -- Contents -- The neurobiology of pain -- John C. Liebeskind (1935â€?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 
505 8 |a 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? 
505 8 |a 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 
505 8 |a 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 
505 8 |a 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 
588 0 |a Print version record. 
590 |a ProQuest Ebook Central  |b Ebook Central Academic Complete 
650 0 |a Neurobiology  |v Congresses. 
650 0 |a Nociceptors  |v Congresses. 
650 0 |a Pain perception  |v Congresses. 
650 0 |a Sodium channels  |v Congresses. 
650 0 |a Ion channels  |v Congresses. 
700 1 |a Liebeskind, John C. 
700 1 |a Dubner, Ronald. 
700 1 |a Gold, Michael Robert. 
710 2 |a National Academy of Sciences (U.S.) 
730 0 |a Proceedings of the National Academy of Sciences of the United States of America. 
740 0 |a Colloquium on the Neurobiology of Pain. 
740 0 |a Colloquium on Neurobiology of Pain. 
776 0 8 |i Print version:  |a National Academy of Sciences Colloquium on the Neurobiology of Pain (1998 : Irvine, Calif.).  |t Papers from a National Academy of Sciences Colloquium on the Neurobiology of Pain.  |d Washington, D.C. : National Academy of Sciences, [1999]  |w (OCoLC)54038127 
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