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Papers from a National Academy of Sciences Colloquium on the Neurobiology of Pain / [organized by John Liebeskind, Ronald Dubner and Michael Gold].

By: Contributor(s): Material type: TextTextSeries: National Academy of Sciences colloquium seriesPublication details: Washington, D.C. : National Academy of Sciences, [1999]Description: 1 online resource (pages 7627-7755) : illustrationsContent type:
  • text
Media type:
  • computer
Carrier type:
  • online resource
ISBN:
  • 0309569338
  • 9780309569330
Other title:
  • Neurobiology of pain
Uniform titles:
  • Proceedings of the National Academy of Sciences of the United States of America.
Subject(s): Genre/Form: Additional physical formats: Print version:: Papers from a National Academy of Sciences Colloquium on the Neurobiology of Pain.DDC classification:
  • 616.0472 22
LOC classification:
  • RB127 .P37 1999eb
Online resources:
Contents:
COLLOQUIUM ON NEUROBIOLOGY OF PAIN -- NATIONAL ACADEMY OF SCIENCES Colloquium Series -- List of Attendees -- Contents -- The neurobiology of pain -- John C. Liebeskind (1935�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
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" ... 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.

Includes bibliographical references.

Print version record.

COLLOQUIUM ON NEUROBIOLOGY OF PAIN -- NATIONAL ACADEMY OF SCIENCES Colloquium Series -- List of Attendees -- Contents -- The neurobiology of pain -- John C. Liebeskind (1935�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

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