title: Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages.
abstract: To examine the pathomechanism of entrapment neuropathy associated with diabetes with special emphasis on the roles of mast cells and Tenascin-C using a rat model of Streptozotocin-induced diabetes. The roles of mast cells and Tenascin-C in development of tarsal tunnel syndrome were analyzed electrophysiologically and histologically in 20 male Ws/Ws-/-rats (mast cell deficient) and 20 of their male wild type counterparts (12-16 weeks old; 250-300 g). Rats were assigned randomly to one of the following three groups; diabetic group and nondiabetic group reared in cages with a wire grid flooring; non-diabetic group in cages with sawdust covered plastic flooring. No significant role for mast cells in entrapment neuropathy was found in the rats with streptozotocin-induced diabetes. Distal latency was prolonged in diabetic rats compared with nondiabetic rats, and positively correlated with increases in blood glucose levels. Tenascin-C expression levels in the endoneurium at the tarsal tunnel in diabetic rats were found to be correlated with distal latency. The anti-alpha-smooth muscle actin (alpha-SMA) positive myofibroblast was scattered in nerve fascicles overexpressing Tenascin-C. It seems likely that Tenascin-C expressing myofibroblasts constrict axons by inducing collagen contraction of the endoneurium. Our data indicate that metabolic and phenotypic abnormalities of endoneurium and perineum lie behind the vulnerability of diabetic patients to entrapment neuropathy.
authors.affiliation: Department of Orthopaedic Surgery, Mie University Faculty of Medicine, Tsu, Mie, Japan. nishit41@pref.mie.jp
authors.forename: Toshiko
authors.initials: T
authors.lastname: Nishimura
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Hirata
authors.forename: Masaya
authors.initials: M
authors.lastname: Tsujii
authors.forename: Ryu
authors.initials: R
authors.lastname: Iida
authors.forename: Yoko
authors.initials: Y
authors.lastname: Hoki
authors.forename: Takahiro
authors.initials: T
authors.lastname: Iino
authors.forename: Satoru
authors.initials: S
authors.lastname: Ogawa
authors.forename: Atsumasa
authors.initials: A
authors.lastname: Uchida
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D001786:Blood Glucose / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D003929:Diabetic Neuropathies / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D004594:Electrophysiology; D019084:Fluorescent Antibody Technique, Indirect; D020868:Gene Silencing; D006614:Hindlimb / Q000294:innervation; D006799:Housing, Animal; D008297:Male; D009408:Nerve Compression Syndromes / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D009431:Neural Conduction; D010525:Peripheral Nerves / Q000378:metabolism / Q000473:pathology; D051381:Rats; D011930:Reaction Time; D019063:Tenascin / Q000378:metabolism; D013979:Tibial Nerve / Q000473:pathology* / Q000503:physiopathology
chemical_list: D001786:Blood Glucose; D019063:Tenascin