附註:" ... 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.
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
