2016
DOI: 10.1055/s-0042-103750
|View full text |Cite
|
Sign up to set email alerts
|

Evaluation of Electrophysiological Effects of Melatonin and Alpha Lipoic Acid in Rats with Streptozotocine Induced Diabetic Neuropathy

Abstract: Our study is the study in which both tibial nerve conduction and cortical tibial SEP studies were performed to compare effects of ALA and melatonin on experimental diabetic neuropathy. Lack of significant difference on cortical tibial SEP study would be attributed to the involvement of other central nervous system pathways which do not include ALA or melatonin in the pathogenesis. RESULTS of ALA group are important by means of giving objective evidences for results of biochemical studies about the role of ALA … Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

1
8
0

Year Published

2017
2017
2021
2021

Publication Types

Select...
7

Relationship

0
7

Authors

Journals

citations
Cited by 12 publications
(9 citation statements)
references
References 26 publications
1
8
0
Order By: Relevance
“…As mentioned previously, high glucose induces oxidative stress and increases Ca 2+ ion entry playing important roles in the pathogenesis of diabetic neuropathy [152]. Treatment with melatonin improves hippocampal injury and peripheral neuropathic pain in STZ-induced diabetic rats; these protective activities of melatonin are characterized by the improvement in the spatial navigation memory and results from electrophysiological studies including tibial motor nerve conduction and cortical tibial nerve somatosensory evoked potentials [153][154][155]. Melatonin inhibits oxidative stress-induced Ca 2+ mobilization through transient receptor potential (TRP) melastatin 2 (TRPM2) and TRP vanilloid type 1 (TRPV1) channels resulting in the prevention of mitochondrial depolarization, intracellular ROS production and apoptosis in neurons [153].…”
Section: Therapeutic Potentials Of Melatonin For Diabetic Neuropathymentioning
confidence: 89%
“…As mentioned previously, high glucose induces oxidative stress and increases Ca 2+ ion entry playing important roles in the pathogenesis of diabetic neuropathy [152]. Treatment with melatonin improves hippocampal injury and peripheral neuropathic pain in STZ-induced diabetic rats; these protective activities of melatonin are characterized by the improvement in the spatial navigation memory and results from electrophysiological studies including tibial motor nerve conduction and cortical tibial nerve somatosensory evoked potentials [153][154][155]. Melatonin inhibits oxidative stress-induced Ca 2+ mobilization through transient receptor potential (TRP) melastatin 2 (TRPM2) and TRP vanilloid type 1 (TRPV1) channels resulting in the prevention of mitochondrial depolarization, intracellular ROS production and apoptosis in neurons [153].…”
Section: Therapeutic Potentials Of Melatonin For Diabetic Neuropathymentioning
confidence: 89%
“…Evidence related to changes in nerve conduction velocity after thioctic acid administration was observed primarily in experimental models [ 58 60 ].…”
Section: Discussionmentioning
confidence: 99%
“…In fact, melatonin has been shown to have substantial analgesic effects [ 17 , 18 , 19 ], and its pain modulatory properties are generally recognised e.g., [ 20 , 21 , 22 , 23 ]. Nevertheless, the involvement of melatonin in neuropathic pain regulation is not fully understood, and is only sparingly mentioned e.g., [ 18 , 24 , 25 , 26 , 27 ]. In particular, only three of the reports regard the peripheral structures that could be promising targets for pain relief.…”
Section: Introductionmentioning
confidence: 99%