Rodella L, Rezzani R, Corsetti G, Bianchi R
Department of Biomedical Sciences and Biotechnology, Division of Human Anatomy, University of Brescia, Via Valsabbina 19, 25124, Brescia, Italy.
Brain Res. 2000 May 19;865(1):112-5. doi: 10.1016/s0006-8993(00)02235-6.
Trigeminal hyperalgesia frequently appears in diabetic neuralgia altering the transmission of orofacial sensory information. This study was designed to explore the effects of trigeminal hyperalgesia in streptozotocin-induced diabetes monitoring the expression of nitric oxide synthase in the trigeminal ganglion cells. The threshold to heat noxious stimuli decreased in diabetic animals. The number of NADPH-diaphorase (NADPH-d)-positive neurons significantly decreased in the diabetic rats compared with controls. Insulin treatment prevented the decreased nociceptive threshold and reduction of the number of NADPH-d-positive neurons. These findings point out that there is a relationship between the trigeminal nociceptive perception and NADPH-d neuronal expression suggesting that NO may play a role in the pathogenesis of trigeminal sensory neuropathy.
三叉神经痛觉过敏经常出现在糖尿病性神经痛中，改变口腔面部感觉信息的传递。本研究旨在探讨链脲佐菌素诱导的糖尿病中三叉神经痛觉过敏的影响，监测三叉神经节细胞中一氧化氮合酶的表达。糖尿病动物对热伤害性刺激的阈值降低。与对照组相比，糖尿病大鼠中烟酰胺腺嘌呤二核苷酸磷酸黄递酶（NADPH-d）阳性神经元的数量显著减少。胰岛素治疗可防止伤害性阈值降低和NADPH-d阳性神经元数量减少。这些发现指出，三叉神经伤害性感受与NADPH-d神经元表达之间存在关联，提示一氧化氮可能在三叉神经感觉神经病变的发病机制中起作用。
