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Open Access Green as soon as Postprint is submitted to ZB.
STZ causes depletion of immune cells in sciatic nerve and dorsal root ganglion in experimental diabetes.
J. Neuroimmunol. 306, 76-82 (2017)
Streptozotocin (STZ) treatment, a common model for inducing diabetes in rodent models, induces thermal hyperalgesia and neuronal toxicity independently of hyperglycemia by oxidizing and activating TRPA1 and TRPV1. Following treatment with STZ, CD45+ immune cells were found to be depleted in sciatic nerve (SN) and DRG in mice, prior to hyperglycemia. Macrophages were also lost in DRG and NFκB-p65-activation was increased in SN macrophages. Immune cells were significantly reduced in both SN and DRG up to three weeks, post-treatment. Loss of PNS-resident macrophages in response to STZ-mediated toxicity may affect the regenerative capacity of the nerve in response to further injury caused by diabetes.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Diabetic Neuropathy ; Experimental Diabetes ; Macrophage ; Neurotoxicity; Thermal Hyperalgesia; Scavenger-receptor; Sensitive Method; Spinal-cord; Streptozotocin; Macrophages; Neuropathy; Pain; Regeneration; Expression
ISSN (print) / ISBN
0165-5728
e-ISSN
1872-8421
Journal
Journal of Neuroimmunology
Quellenangaben
Volume: 306,
Pages: 76-82
Publisher
Elsevier
Publishing Place
Amsterdam
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Cancer (IDC)