Bradykinin Produces Pain Hypersensitivity by Potentiating Spinal Cord Glutamatergic Synaptic Transmission

• DOI: 10.1523/jneurosci.2393-05.2005
• Publication Date: 2005-08-31T19:18:36Z
• Authors: Haibin Wang; Tatsuro Kohno; Fumimasa Amaya; Gary J. Brenner; Nobuko Ito; Andrew Allchorne; Ru-Rong Ji; Clifford J. Woolf
• Keywords: Nociceptor; Dorsal root ganglion

Bradykinin, an inflammatory mediator, sensitizes nociceptor peripheral terminals reducing pain threshold. We now show that the B 2 kinin receptor is expressed in rat dorsal horn neurons and bradykinin, a -specific agonist, augments AMPA- NMDA-induced, primary afferent-evoked EPSCs, increases frequency amplitude of miniature EPSCs superficial vitro . Administration bradykinin to spinal cord vivo produces, moreover, NMDA-dependent hyperalgesia. also demonstrate nociceptive inputs result production intrathecal -selective antagonist suppresses behavioral manifestations central sensitization, activity-dependent increase glutamatergic synaptic efficacy. Primary sensitization is, addition, reduced knock-out mice. conclude released response acts as neuromodulator, potentiating transmission produce hypersensitivity.