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Science 9 June 2000: Vol. 288. no. 5472, pp. 1765 - 1768 DOI: 10.1126/science.288.5472.1765
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Review
Neuronal Plasticity: Increasing the Gain in Pain
Clifford J. Woolf,
1*
Michael W. Salter
2
We describe those sensations that are unpleasant, intense, or
distressing as painful. Pain is not homogeneous, however, and comprises
three categories: physiological, inflammatory, and neuropathic pain.
Multiple mechanisms contribute, each of which is subject to or an
expression of neural plasticity--the capacity of neurons to change
their function, chemical profile, or structure. Here, we develop a
conceptual framework for the contribution of plasticity in primary
sensory and dorsal horn neurons to the pathogenesis of pain,
identifying distinct forms of plasticity, which we term activation,
modulation, and modification, that by increasing gain, elicit
pain hypersensitivity.
1 Neural Plasticity Research Group, Department
of Anesthesia and Critical Care, Massachusetts General Hospital and
Harvard Medical School, MGH-East, Charlestown, MA 02129, USA.
2 Program in Brain and Behaviour, Hospital for Sick
Children and University of Toronto Centre for the Study of Pain,
Toronto, Ontario M5G 1X8, Canada.
*
To whom correspondence should be addressed. E-mail:
woolf.clifford{at}mgh.harvard.edu
Read the Full Text
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- Blocking Caspase Activity Prevents Transsynaptic Neuronal Apoptosis and the Loss of Inhibition in Lamina II of the Dorsal Horn after Peripheral Nerve Injury.
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- Migraine: New Molecular Mechanisms.
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