Liu J, Wang K M, He L Z, Cao D Y
Department of Brain and Nerve, Xian Medical University.
Sheng Li Xue Bao. 1996 Dec;48(6):536-42.
While sympathetic efferents and prostaglandins (PGs) play an important role in hyperalgesia of partial injury of peripheral nerves and inflammation, whether these are also involved in diabetic hyperalgesia is unknown. With intraperitoneal injection of 6-hydroxydopamine (6-OHDA) to eliminate effects of sympathetic postganglionic neurons (SPGNs) terminals, a model of diabetic rats with infused 6-OHDA could be set up by injection of streptozotocin (STZ). Nociceptive paw-withdrawal threshold (NPWT) and tail flick latency (TFL) in 6-OHDA/diabetic rats were not changed significantly in the following four weeks. However, in diabetic group rats, pain threshold was decreased significantly and accompanied by development of hyperalgesia. NPWT was significantly decreased with noradrenaline (NA) in diabetic hyperalgesic rats and increased with phentolamine or yohimbine, but not by prazocin. In the control rats, NPWT are not changed significantly by NA or phentolamine, and in 6-OHDA/diabetic rats, neither NA nor phentolamine also affected on NPWT significantly. However, NPWT may be significantly decreased by PGE1, PGE2 and PGD2 in both the control and the diabetic hyperalgesic rats. The above results suggested that SPGNs terminals are involved in hyperalgesia of diabetic rats, NA accelerated synthesis of PGs and released by way of presynaptic effect on alpha 2-adrenergic receptors at the SPGNs terminals, PGs, in turn, directly acted on the primary afferent nociceptors, producing hyperalgesia.
