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

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

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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.
Subjects:
Neurobiology > Congresses.
Nociceptors > Congresses.
Pain perception > Congresses.
Sodium channels > Congresses.
Ion channels > Congresses.
Local Note:ProQuest Ebook Central
Table of Contents:
  • 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
  • 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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