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• W1498016779 abstract "Abstract Nociceptive primary afferents have the capacity to induce a state of increased excitability in dorsal horn neurons of the spinal cord or central sensitization causing thermal hyperalgesia and touch‐evoked pain (allodynia). It is believed that primary afferent C‐fibres become hypersensitive and induce hyperalgesia and that low‐threshold Aβ‐fibres are responsible for induction of allodynia, the mechanisms of which remain elusive. We previously showed that intrathecal administration of prostaglandin E 2 (PGE 2 ) and prostaglandin F 2α (PGF 2α ) induce allodynia in conscious mice. Here we demonstrated that selective elimination of C‐fibres by neonatal capsaicin treatment resulted in the disappearance of allodynia induced by PGE 2 , but not that by PGF 2α . PGE 2 ‐induced allodynia was not observed in N‐methyl‐D‐aspartate (NMDA) receptor ε1 subunit knockout mice and was sensitive to morphine. In contrast, PGF 2α ‐induced allodynia was not observed in NMDA ε4 subunit knockout mice and was insensitive to morphine. Furthermore, while PGF 2α showed a capsaicin‐insensitive feeble facilitatory action on evoked excitatory postsynaptic currents in dorsal horn neurons, PGE 2 induced a long‐lasting facilitation of evoked excitatory postsynaptic currents in a capsaicin‐sensitive manner. Taken together, the present study demonstrates that there are two pathways for induction of allodynia and that capsaicin‐sensitive C‐fibres may participate in PGE 2 ‐induced allodynia." @default.
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• W1498016779 date "1999-06-01" @default.
• W1498016779 modified "2023-10-17" @default.
• W1498016779 title "Involvement of primary afferent C-fibres in touch-evoked pain (allodynia) induced by prostaglandin E₂" @default.
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• W1498016779 doi "https://doi.org/10.1046/j.1460-9568.1999.00602.x" @default.
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