Alterations in the neural circuits from peripheral afferents to the spinal cord: possible implications for diabetic polyneuropathy in streptozotocin-induced type 1 diabetic rats
Autor: | Hui Li, Yun-Qing Li, Zhen-Yu Wu, Jia-Chen Hu, Juan Qu, Chun-Yu Li, Tan Ding, Yong-Hui Liao, Dong-Liang Zhang, Zhen-Zhen Kou, Jun-Bin Yin |
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Rok vydání: | 2014 |
Předmět: |
Male
Pain Threshold dorsal root ganglion Calcitonin Gene-Related Peptide Cognitive Neuroscience medicine.medical_treatment Neuroscience (miscellaneous) neural circuit Motor Activity Calcitonin gene-related peptide lcsh:RC321-571 Diabetes Mellitus Experimental Rats Sprague-Dawley Cellular and Molecular Neuroscience diabetic polyneuropathy Diabetic Neuropathies Dorsal root ganglion Ganglia Spinal Lectins Diabetes mellitus medicine Animals rat Original Research Article Neurons Afferent lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry business.industry Insulin spinal cord Streptozotocin Spinal cord medicine.disease primary afferent Sensory Systems Rats Diabetes Mellitus Type 1 medicine.anatomical_structure Calcitonin Spinal nerve Nerve Net business Neuroscience medicine.drug |
Zdroj: | Frontiers in Neural Circuits Frontiers in Neural Circuits, Vol 8 (2014) |
ISSN: | 1662-5110 |
Popis: | 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. |
Databáze: | OpenAIRE |
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