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R. Dubner

Bio: R. Dubner is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Neuropeptide & Dynorphin. The author has an hindex of 1, co-authored 1 publications receiving 930 citations.

Papers
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Journal ArticleDOI
TL;DR: A model has been proposed in which dynorphin, substance P and calcitonin gene-related peptide enhance excitability at NMDA receptor sites, leading first to dorsal horn hyperexcitability and then to excessive depolarization and excitotoxicity.

936 citations


Cited by
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Journal ArticleDOI
TL;DR: The present review focuses on the organisation of descending pathways and their pathophysiological significance, the role of individual transmitters and specific receptor types in the modulation and expression of mechanisms of descending inhibition and facilitation and the advantages and limitations of established and innovative analgesic strategies which act by manipulation of descending controls.

2,565 citations

Journal ArticleDOI
01 Mar 1993-Pain
TL;DR: This review examines the clinical and experimental evidence which points to a contribution of central Neurol plasticity to the development of pathological pain, and assesses the physiological, biochemical, cellular and molecular mechanisms that underlie plasticity induced in the central nervous system in response to noxious peripheral stimulation.
Abstract: Peripheral tissue damage or nerve injury often leads to pathological pain processes, such as spontaneous pain, hyperalgesia and allodynia, that persist for years or decades after all possible tissue healing has occurred. Although peripheral neural mechanisms, such as nociceptor sensitization and neuroma formation, contribute to these pathological pain processes, recent evidence indicates that changes in central neural function may also play a significant role. In this review, we examine the clinical and experimental evidence which points to a contribution of central neural plasticity to the development of pathological pain. We also assess the physiological, biochemical, cellular and molecular mechanisms that underlie plasticity induced in the central nervous system (CNS) in response to noxious peripheral stimulation. Finally, we examine theories which have been proposed to explain how injury or noxious stimulation lead to alterations in CNS function which influence subsequent pain experience.

1,974 citations

Journal ArticleDOI
TL;DR: A global account of mechanisms involved in the induction of pain is provided, including neuronal pathways for the transmission of nociceptive information from peripheral nerve terminals to the dorsal horn, and therefrom to higher centres.

1,752 citations

Journal ArticleDOI
TL;DR: This article reviews findings up to the end of 1997 about the inducible transcription factors c-Jun, JunB, JunD, c-Fos, FosB, Fra,1, Fra-2, Krox-20 (Egr-2) and Krox -24 (NGFI-A, Egr-1, Zif268) as they pertain to gene expression in the mammalian nervous system and describes their expression and possible roles in glial cells.

1,361 citations

Journal ArticleDOI
TL;DR: Analysis of the molecular mechanisms underlying the generation and maintenance of central sensitization and LTP indicates that, although there are differences between the synaptic plasticity contributing to memory and pain, there are also striking similarities.

1,361 citations