| First Author | Rácz I | Year | 2005 |
| Journal | Neuroreport | Volume | 16 |
| Issue | 18 | Pages | 2025-8 |
| PubMed ID | 16317347 | Mgi Jnum | J:103696 |
| Mgi Id | MGI:3610627 | Doi | 10.1097/00001756-200512190-00011 |
| Citation | Racz I, et al. (2005) Visceral, inflammatory and neuropathic pain in glycine receptor alpha 3-deficient mice. Neuroreport 16(18):2025-8 |
| abstractText | The alpha3-subunit of strychnine-sensitive glycine receptors is an important modulator of the pain-sensitizing effects of spinal prostaglandin prostaglandin E(2). Mice deficient for alpha3-subunit of strychnine-sensitive glycine receptors lack the prostaglandin E(2)-induced inhibition of glycinergic neurotransmission and recover faster from inflammation-induced hyperalgesia. It, however, remains unclear whether alpha3-subunit of strychnine-sensitive glycine receptors plays a role in other pain models involving prostaglandin synthesis, such as chemically induced pain or neuropathic pain. In this paper, we show a reduction of acetic acid-induced writhing responses in the absence of alpha3-subunit of strychnine-sensitive glycine receptors, but no changes in formalin-induced pain. Furthermore, alpha3-subunit of strychnine-sensitive glycine receptors-deficient mice develop normal thermal hyperalgesia and tactile allodynia. Thus, alpha3-subunit of strychnine-sensitive glycine receptors is involved in the modulation of moderate inflammatory acetic acid-induced pain responses, but neither in formalin-induced pain nor in neuropathic pain. |
