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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Action Potentials / drug effects
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Animals
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Calcium / metabolism
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Calcium Channels, T-Type / metabolism*
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Excitatory Postsynaptic Potentials
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Hyperalgesia / physiopathology*
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Ion Channel Gating
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Long-Term Potentiation*
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Membrane Potentials
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Nerve Fibers, Unmyelinated / physiology
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Neurokinin-1 Receptor Antagonists
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Nickel / pharmacology
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Patch-Clamp Techniques
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Posterior Horn Cells / metabolism
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Posterior Horn Cells / physiology*
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Quinuclidines / pharmacology
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Rats
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Rats, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate / metabolism
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Receptors, Neurokinin-1 / metabolism*
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Signal Transduction
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Substance P / pharmacology
Substances
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Calcium Channels, T-Type
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Neurokinin-1 Receptor Antagonists
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Quinuclidines
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Receptors, N-Methyl-D-Aspartate
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Receptors, Neurokinin-1
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L 703606
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Substance P
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Nickel
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Calcium