Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia.
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.
Ikeda
Hiroshi
H
Institute of Physiology and Pathophysiology, Heidelberg University, D-69120 Heidelberg, Germany.
Heinke
Bernhard
B
Ruscheweyh
Ruth
R
Sandkühler
Jurgen
J
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism; D020747:Calcium Channels, T-Type / Q000378:metabolism*; D019706:Excitatory Postsynaptic Potentials; D006930:Hyperalgesia / Q000503:physiopathology*; D015640:Ion Channel Gating; D017774:Long-Term Potentiation; D008564:Membrane Potentials; D036421:Nerve Fibers, Unmyelinated / Q000502:physiology; D064729:Neurokinin-1 Receptor Antagonists; D009532:Nickel / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D020671:Posterior Horn Cells / Q000378:metabolism / Q000502:physiology*; D011812:Quinuclidines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D018040:Receptors, Neurokinin-1 / Q000378:metabolism*; D015398:Signal Transduction; D013373:Substance P / Q000494:pharmacology
D020747:Calcium Channels, T-Type; D064729:Neurokinin-1 Receptor Antagonists; D011812:Quinuclidines; D016194:Receptors, N-Methyl-D-Aspartate; D018040:Receptors, Neurokinin-1; C076851:L 703606; D013373:Substance P; D009532:Nickel; D002118:Calcium