Synaptic Plasticity in Spinal Lamina I Projection Neurons That Mediate Hyperalgesia
作者： H. Ikeda
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摘要: 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 neurokinin 1 receptor for substance P mediate this abnormal pain by unknown cellular mechanism. We report these, but not other nociceptive cells, receptor-activated signal transduction pathways and activation low-threshold (T-type) voltage-gated calcium channels synergistically facilitate activity- calcium-dependent long-term potentiation at synapses from fibers. Thereby, memory traces events are retained.
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