Abstract
Diabetic polyneuropathy (DPN) presents as a wide variety of sensorimotor symptoms and affects approximately 50% of diabetic patients. Changes in the neural circuits may occur in the early stages in diabetes and are implicated in the development of DPN. Therefore, we aimed to detect changes in the expression of isolectin B4 (IB4, the marker for nonpeptidergic unmyelinated fibers and their cell bodies) and calcitonin gene-related peptide (CGRP, the marker for peptidergic fibers and their cell bodies) in the dorsal root ganglion (DRG) and spinal cord of streptozotocin (STZ)-induced type 1 diabetic rats showing alterations in sensory and motor function. We also used cholera toxin B subunit (CTB) to show the morphological changes of the myelinated fibers and motor neurons. STZ-induced diabetic rats exhibited hyperglycemia, decreased body weight gain, mechanical allodynia and impaired locomotor activity. In the DRG and spinal dorsal horn, IB4-labeled structures decreased, but both CGRP immunostaining and CTB labeling increased from day 14 to day 28 in diabetic rats. In spinal ventral horn, CTB labeling decreased in motor neurons in diabetic rats. Treatment with intrathecal injection of insulin at the early stages of DPN could alleviate mechanical allodynia and impaired locomotor activity in diabetic rats. The results suggest that the alterations of the neural circuits between spinal nerve and spinal cord via the DRG and ventral root might be involved in DPN.
Highlights
Diabetic polyneuropathy (DPN) is one of the most common complications of diabetes mellitus (DM; Dyck et al, 1993)
CHANGES IN ISOLECTIN B4 (IB4)-LABELED AND CALCITONIN GENE-RELATED PEPTIDE (CGRP)-IMMUNOREACTIVE STRUCTURES IN THE DORSAL ROOT GANGLION (DRG) AND SPINAL DORSAL HORN To investigate whether the nonpeptidergic unmyelinated fibers and their cell bodies, and the peptidergic fibers and their cell bodies are involved in DPN, we examined the IB4-labeled and CGRP-immunoreactive (IR) structures in the DRG and spinal dorsal horn
Our results show that STZ-induced diabetic rats exhibit hyperglycemia, decreased body weight gain and mechanical allodynia after STZ injection, as well as impaired locomotor activity at day 28, supporting the use of STZ-induced diabetic rats as an animal model for studying the mechanism of the early stages of type 1 DPN
Summary
Diabetic polyneuropathy (DPN) is one of the most common complications of diabetes mellitus (DM; Dyck et al, 1993). A large proportion of diabetic patients who suffer from DPN describe abnormal sensations such as pain in the early stages. Painful DPN in human subjects is usually characterized by the development of tactile allodynia, a condition in which light touch is perceived as painful (Baron et al, 2009). Tactile allodynia is observed in a large proportion (30–47%) of human subjects with DM (Bastyr et al, 2005). In contrast to sensory disturbance, motor function has rarely been studied in DPN (Andersen, 2012). Previous reports demonstrate that type 1 diabetic patients exhibit impaired strength of the ankle and knee extensors and flexors, indicating that DPN is often a mixed sensory-motor neuropathy (Andersen, 2012; IJzerman et al, 2012). Despite considerable research on DPN, evidence for pathophysiological changes in the nervous systems underlying the impairment of motor function still lacks neurostructural evidence
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
