Frontiers in neural circuits, 2014, Vol.8, p.6-6
2014
Details
- Autor(en) / Beteiligte
- Titel
- Alterations in the neural circuits from peripheral afferents to the spinal cord: possible implications for diabetic polyneuropathy in streptozotocin-induced type 1 diabetic rats
- Ist Teil von
- Frontiers in neural circuits, 2014, Vol.8, p.6-6
- Ort / Verlag
- Switzerland: Frontiers Research Foundation
- Erscheinungsjahr
- 2014
- Link zum Volltext
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1662-5110eISSN: 1662-5110DOI: 10.3389/fncir.2014.00006Titel-ID: cdi_doaj_primary_oai_doaj_org_article_5c36579dff2346c98a11dc6e04809147
- Format
- –
- Schlagworte
- Animals, Body weight gain, Calcitonin, Calcitonin gene-related peptide, Calcitonin Gene-Related Peptide - metabolism, Cholera, Cholera toxin, Cholera toxin B subunit, Circuits, Diabetes, Diabetes mellitus, Diabetes Mellitus, Experimental - metabolism, Diabetes Mellitus, Experimental - physiopathology, Diabetes Mellitus, Type 1 - metabolism, Diabetes Mellitus, Type 1 - physiopathology, Diabetic Neuropathies - metabolism, Diabetic Neuropathies - physiopathology, Diabetic neuropathy, Diabetic polyneuropathy, Dorsal horn, Dorsal root ganglia, Dorsal root ganglion, Fibers, Ganglia, Spinal - metabolism, Ganglia, Spinal - physiopathology, Human subjects, Hyperglycemia, Insulin, Laboratory animals, Lectins - metabolism, Locomotor activity, Male, Motor Activity - physiology, Motor neurons, Nerve Net - metabolism, Nerve Net - physiopathology, neural circuit, Neural networks, Neurons, Afferent - metabolism, Neurons, Afferent - physiology, Neuroscience, Neurosciences, Pain, Pain perception, Pain Threshold - physiology, Peptides, Polyneuropathy, primary afferent, rat, Rats, Rats, Sprague-Dawley, Rodents, Sensorimotor system, Spinal Cord, Spinal Cord - metabolism, Spinal Cord - physiopathology, Spinal nerves, Streptozocin, Ventral roots