| First Author | Kallenborn-Gerhardt W | Year | 2012 |
| Journal | Behav Brain Res | Volume | 226 |
| Issue | 1 | Pages | 106-11 |
| PubMed ID | 21924294 | Mgi Jnum | J:177731 |
| Mgi Id | MGI:5295907 | Doi | 10.1016/j.bbr.2011.09.002 |
| Citation | Kallenborn-Gerhardt W, et al. (2012) Prolonged zymosan-induced inflammatory pain hypersensitivity in mice lacking glycine receptor alpha2. Behav Brain Res 226(1):106-11 |
| abstractText | Glycinergic synapses play a major role in shaping the activity of spinal cord neurons under normal conditions and during persistent pain. However, the role of different glycine receptor (GlyR) subtypes in pain processing has only begun to be unraveled. Here, we analysed whether the GlyR alpha2 subunit might be involved in the processing of acute or persistent pain. Real-time RT-PCR and in situ hybridization analyses revealed that GlyR alpha2 mRNA is enriched in the dorsal horn of the mouse spinal cord. Mice lacking GlyR alpha2 (Glra2(-/-) mice) demonstrated a normal nociceptive behavior in models of acute pain and after peripheral nerve injury. However, mechanical hyperalgesia induced by peripheral injection of zymosan was significantly prolonged in Glra2(-/-) mice as compared to wild-type littermates. We conclude that spinal GlyRs containing the alpha2 subunit exert a previously unrecognized role in the resolution of inflammatory pain. |
