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 E2 (PGE2) and prostaglandin F2α (PGF2α) 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 PGE2, but not that by PGF2α. PGE2-induced allodynia was not observed in N-methyl-D-aspartate (NMDA) receptor ε1 subunit knockout mice and was sensitive to morphine. In contrast, PGF2α-induced allodynia was not observed in NMDA ε4 subunit knockout mice and was insensitive to morphine. Furthermore, while PGF2α showed a capsaicin-insensitive feeble facilitatory action on evoked excitatory postsynaptic currents in dorsal horn neurons, PGE2 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 PGE2-induced allodynia.