doi: 10.1126/science.1080659.
Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia
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- PMID: 12595694
- DOI: 10.1126/science.1080659
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Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia
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Abstract
Inflammation, trauma, or nerve injury may cause enduring hyperalgesia, an enhanced sensitivity to painful stimuli. Neurons in lamina I of the spinal dorsal horn that express the neurokinin 1 receptor for substance P mediate this abnormal pain sensitivity by an unknown cellular mechanism. We report that in these, but not in other nociceptive lamina I cells, neurokinin 1 receptor-activated signal transduction pathways and activation of low-threshold (T-type) voltage-gated calcium channels synergistically facilitate activity- and calcium-dependent long-term potentiation at synapses from nociceptive nerve fibers. Thereby, memory traces of painful events are retained.
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