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Inflammation, trauma, or nerve injury may cause enduring
hyperalgesia, an enhanced sensitivity to painful stimuli. Neuronsin
lamina I of the spinal dorsal horn that express the neurokinin1 receptor for substance P mediate this abnormal pain sensitivityby an
unknown cellular mechanism. We report that in these, butnot in other
nociceptive lamina I cells, neurokinin 1 receptor-activatedsignal
transduction pathways and activation of low-threshold (T-type)voltage-gated calcium channels synergistically facilitate activity-and
calcium-dependent long-term potentiation at synapses fromnociceptive
nerve fibers. Thereby, memory traces of painful eventsare retained.
1 Institute of Physiology and Pathophysiology,
Heidelberg University, D-69120 Heidelberg, Germany.
2 Brain Research Institute, Vienna University
Medical School, A-1090 Vienna, Austria.
*
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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