Pain sensing is an important nervous system function to detect and avoid potentially harmful stimuli. In addition to direct noxious stimuli, inflammation and neuronal damage can also raise sensory nerve activation which is then transmitted to a higher brain region through particular neural pathways. In addition, pain sensing is increased under various physiological or pathological conditions such as viral infection, diabetes, cancer, chronic inflammation, or damage to neuronal fibers. It is possible that pain sensitivity persists long after tissue injury or inflammation has been resolved. In this chronic case, pain is a disease rather than a sign of tissue damage because pain sensitivity without tissue damage is not beneficial in avoidance of further tissue damage. Although the nervous system has abundant gangliosides, which play important roles in neural functions, little is known how gangliosides regulate pain sensing. In this review, we introduce several works that reveal gangliosides modulate pain sensing. These studies involve using naïve animals or pathological animal models. Moreover, we discuss the possibility that peripheral ganglioside GT1b produces nociception and hyperalgesia by regulation of peripheral glutamate signaling.

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This mini-review focuses on the synthesis and biological activities of sialic acid (SA) derivatives with a C-glycosidic linkage in place of the standard O-glycosidic bond at the C-2 position. We summarize reported synthetic methodologies for mono- and di-saccharides in separate sections. Then, we introduce our strategy for the construction of C-sialoside linkages utilizing Ireland–Claisen rearrangement reaction and its application to the synthesis of a ganglioside GM4 analogue. Although C-sialosides are expected to be useful as sialidase-resistant analogues of sialoglycoconjugates (sialoGCs), their biological activities have not yet been investigated in detail. Herein we briefly discuss the potential applications of C-sialosides.

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