Glycosphingolipids (GSLs) are abundant, ceramide-containing lipids in the nervous system that play key functional roles in pain and inflammation. We measured gene expression (Ugcg, St3gal5, St8sia1, B4galNT1, Ugt8a, and Gal3st1) of glycosyltransferases involved in GSL synthesis in murine dorsal root ganglion (DRG) and spinal cord after complete Freund's adjuvant (CFA)-induced unilateral hind-paw inflammation (1 day vs. 15 days). Chronic inflammation (15 days) sensitized both ipsilateral and contralateral paws to pain. One day of induced unilateral hind-paw inflammation (1d-IUHI) increased Ugcg, St8sia1, B4galnt1, and Gal3st1 expression in ipsilateral cord, suggesting that sulfatide and b-series gangliosides were also elevated. In addition, 1d-IUHI increased Ugcg, st3gal5 and Gal3st1 expression in contralateral cord, suggesting that sulfatide and a-/b-series gangliosides were elevated. By contrast, 1d-IUHI decreased Ugcg, St3gal5, and St8sia1 expression bilaterally in the DRG, suggesting that b-series gangliosides were depressed. Since intrathecal injection of b-series ganglioside induced mechanical allodynia in naïve mice, it seems reasonable that b-series gangliosides synthesized from upregulated St8sia1 in the ipsilateral spinal cord are involved in mechanical allodynia. By contrast, chronic inflammation led to a decrease of Ugcg, St3gal5, B4galnt1, and Gal3st1 expression in spinal cord bilaterally and an increase of St8sia1 expression in the ipsilateral DRG, suggesting that a-/b-series gangliosides in the spinal cord decreased and b-series gangliosides in ipsilateral DRG increased. These changes in glycosyltransferase gene expression in the DRG and the spinal cord may contribute to the modification of pain sensitivity in both inflamed and non-inflamed tissues and the transition from early to chronic inflammatory pain.

中文翻译：

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炎性疼痛期间脊髓和背根神经节中糖脂脂的生物合成途径：糖基转移酶基因表达模式的早期和晚期变化。

糖鞘脂（GSLs）是神经系统中大量含有神经酰胺的脂质，在疼痛和炎症中起关键作用。我们在完全弗氏佐剂（CFA）诱导的单侧后爪发炎（CFA）诱导的单侧后爪发炎后，测量了鼠背根神经节（DRG）和脊髓中参与GSL合成的糖基转移酶的基因表达（Ugcg，St3gal5，St8sia1，B4galNT1，Ugt8a和Gal3st1） 1天与15天）。慢性炎症（15天）使同侧和对侧爪子都感到疼痛。一天的诱导性单侧后爪发炎（1d-IUHI）增加了同侧脐带中Ugcg，St8sia1，B4galnt1和Gal3st1的表达，这表明硫化物和b系列神经节苷脂也升高。此外，1d-IUHI增加对侧脐带中Ugcg，st3gal5和Gal3st1的表达，提示硫化物和a- / b系列神经节苷脂水平升高。相比之下，1d-IUHI降低了DRG两侧的Ugcg，St3gal5和St8sia1表达，表明b系列神经节苷脂被抑制。由于鞘内注射b系列神经节苷脂可在幼稚小鼠中引起机械性异常性疼痛，因此从同侧脊髓中St8sia1上调合成的b系列神经节苷脂参与机械性异常性疼痛似乎是合理的。相比之下，慢性炎症导致双侧脊髓Ugcg，St3gal5，B4galnt1和Gal3st1表达减少，同侧DRG中St8sia1表达增加，提示脊髓中a- / b系列神经节苷脂减少，b同侧DRG中的神经节苷脂系列增加。