%0 Journal Article
%T n5-STZ Diabetic Model Develops Alterations in Sciatic Nerve and Dorsal Root Ganglia Neurons of Wistar Rats
%A Francisco Walber Ferreira-da-Silva
%A Kerly Shamyra da Silva-Alves
%A Matheus Lemos-dos-Santos
%A Keciany Alves de Oliveira
%A Humberto Cavalcante Joca
%A Otoni Cardoso do Vale
%A Andrelina Noronha Coelho-de-Souza
%A Jos¨¦ Henrique Leal-Cardoso
%J ISRN Endocrinology
%D 2013
%R 10.1155/2013/638028
%X One experimental model of diabetes mellitus (DM) similar to type II DM, called n5-STZ, is obtained by a single injection (via i.p.) of streptozotocin (STZ) in the 5th day of life of newborn rats. The present investigation aimed to characterize alterations in excitability of rat peripheral neurons in n5-STZ model. n5-STZ DM was induced, and electrophysiological evaluation was done at 12th week of rat life. Rats developed glucose intolerance, sensory alteration, and hyperglycemia or near-normoglycemia ( and £¿mmol/L). In near-normoglycemia group the significant electrophysiological alteration observed was decreased in amplitude of 2nd wave (2nd component, conduction velocity: 48.8£¿m/s) of compound action potential (CAP) of sciatic nerve. For hyperglycemic rats, decreased excitability, amplitude, and conduction velocity of 2nd CAP component of sciatic nerve were found; a depolarization of resting potential (4-5£¿mV) and reduction in maximum ascendant and descendant inclinations of action potential were found in DRG neurons but no alteration on Na+ current ( ). Thus, n5-STZ rats develop alterations in excitability which were related to glycemic levels but were not likely attributable to changes on . Our data confirm that n5-STZ model is a useful model to study type II DM. 1. Introduction Diabetes mellitus (DM) is a metabolic disorder with great worldwide prevalence in adult and elderly population [1]. This disease is characterized mainly by hyperglycemia and insufficient insulin secretion or resistance to insulin by tissues. It is generally classified as type I diabetes, in which there is absolute lack of insulin caused by pancreatic beta cell destruction and type II diabetes, in which there is insufficient insulin secretion or insulin resistance in peripheral tissues [2]. Several complications are associated with DM including retinopathy, nephropathy, and peripheral neuropathy [3]. Neuropathy is the most frequent complication, reaching an incidence up to 50% in cases of long-lasting DM evolutions [4]. Due to the large incidence and debilitating characteristics of DM, animal models have been developed to simulate the symptoms of human diabetes [5]. One of these models is the streptozotocin (STZ-) induced DM, which has been widely used to study diabetic complications. This model presents features that resemble human disease and can be used to induce both type I and type II DM [6, 7]. To induce type I DM, generally adult rats (rat adult model of DM) and doses of STZ, which in one week induce DM with plasma glucose levels >15£¿mmol/L, have been used [7¨C9]. In
%U http://www.hindawi.com/journals/isrn.endocrinology/2013/638028/