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Synaptic Plasticity in Spinal Lamina I Projection Neurons That Mediate Hyperalgesia

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Science  21 Feb 2003:
Vol. 299, Issue 5610, pp. 1237-1240
DOI: 10.1126/science.1080659

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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.

  • * Present address: Department of Human and Artificial Intelligence Systems, Fukui University, Fukui, Japan.

  • To whom correspondence should be addressed. E-mail: juergen.sandkuehler{at}univie.ac.at

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