PMID- 17030435 OWN - NLM STAT- MEDLINE DCOM- 20070104 LR - 20061106 IS - 0304-3940 (Print) IS - 0304-3940 (Linking) VI - 409 IP - 3 DP - 2006 Dec 6 TI - Participation of peripheral group I and II metabotropic glutamate receptors in the development or maintenance of IL-1beta-induced mechanical allodynia in the orofacial area of conscious rats. PG - 173-8 AB - The present study investigated the role of peripheral groups I and II metabotropic glutamate receptors (mGluRs) in interleukin (IL)-1beta-induced mechanical allodynia in the orofacial area of rats. Subcutaneous injection of 10 pg of IL-1beta decreased air-puff thresholds ipsilateral or contralateral to the injection site. The decrease in air-puff thresholds appeared 10 min after the injection of IL-1beta and IL-1beta-induced mechanical allodynia persisted for over 3 h. Pre-treatment with 7-(hydroxyimino) cyclopropa[b] chromen-1a-carboxylate ethyl ester (CPCCOEt) or 2-methyl-6-(phenylethynyl)-pyridine hydrochloride (MPEP), a mGluR1 or mGluR5 antagonist, blocked IL-1beta-induced mechanical allodynia and mirror-image mechanical allodynia produced by a subcutaneous injection of 10 pg of IL-1beta. However, post-treatment with CPCCOEt or MPEP did not affect changes in behavioral responses, which were produced by the IL-1beta injection. Pre-treatment, as well as post-treatment with (2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate (APDC), a group II mGluR agonist, blocked either IL-1beta-induced mechanical allodynia or mirror-image mechanical allodynia. The anti-allodynic effects of APDC were abolished by pre-treatment with (2S)-2-amino-2[(1S,2S)-2-carboxycycloprop-1-yl]-3-(xanth-9-yl) propanoic acid (LY341495), a group II mGluR antagonist. These results indicate that peripheral group II mGluRs are involved in the development and maintenance of IL-1beta-induced mechanical allodynia, while peripheral group I mGluRs are involved in the development of IL-1beta-induced mechanical allodynia. Based on our observations, the peripheral application of group II mGluR agonists may be of therapeutic value in treating inflammatory pain. FAU - Jung, Chang Y AU - Jung CY AD - Department of Oral Physiology and BrainKorea 21, School of Dentistry, Kyungpook University, Daegu, South Korea. FAU - Lee, Sang Y AU - Lee SY FAU - Choi, Hyo S AU - Choi HS FAU - Lim, Eun J AU - Lim EJ FAU - Lee, Min K AU - Lee MK FAU - Yang, Gwi Y AU - Yang GY FAU - Han, Seung R AU - Han SR FAU - Youn, Dong H AU - Youn DH FAU - Ahn, Dong K AU - Ahn DK LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20061006 PL - Ireland TA - Neurosci Lett JT - Neuroscience letters JID - 7600130 RN - 0 (Interleukin-1beta) RN - 0 (Receptors, Metabotropic Glutamate) RN - 0 (metabotropic glutamate receptor 2) RN - 0 (metabotropic glutamate receptor type 1) SB - IM MH - Animals MH - Consciousness MH - Facial Pain/chemically induced/*metabolism MH - Hyperesthesia/chemically induced/*metabolism MH - *Interleukin-1beta MH - Rats MH - Receptors, Metabotropic Glutamate/*metabolism MH - Touch/*drug effects EDAT- 2006/10/13 09:00 MHDA- 2007/01/05 09:00 CRDT- 2006/10/13 09:00 PHST- 2006/07/18 00:00 [received] PHST- 2006/09/18 00:00 [revised] PHST- 2006/09/18 00:00 [accepted] PHST- 2006/10/13 09:00 [pubmed] PHST- 2007/01/05 09:00 [medline] PHST- 2006/10/13 09:00 [entrez] AID - S0304-3940(06)01004-4 [pii] AID - 10.1016/j.neulet.2006.09.043 [doi] PST - ppublish SO - Neurosci Lett. 2006 Dec 6;409(3):173-8. doi: 10.1016/j.neulet.2006.09.043. Epub 2006 Oct 6.