## Abstract Maternal diabetes causes neural tube defects in embryos, which are associated with increased apoptosis in the neuroepithelium. Many factors, including effector caspases, have been shown to be involved in the events. However, the key regulators have not been identified and the underlying
The role of axonal ion conductances in diabetic neuropathy: A review
โ Scribed by Stefan Quasthoff
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 141 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0148-639X
No coin nor oath required. For personal study only.
โฆ Synopsis
Diabetic neuropathy is a common complication in diabetes mellitus. Diabetic neuropathy is accompanied by alterations in axonal excitability, which can lead to either ''positive'' (paresthesia, dysesthesia, pain) and/or ''negative'' (hypesthesia, anesthesia) symptoms. The mechanisms underlying these alterations in axonal excitability are not well understood. Clinical tests reveal reduced nerve conduction velocity and axonal loss, but fail to explain nerve excitability. Many different factors have been suggested in relation to the pathophysiology of diabetic neuropathy. There are probably as many factors as there are different clinical pictures in diabetic neuropathy. Nevertheless, it seems that hyperglycemic hypoxia is mainly responsible for the electrophysiological changes seen in damaged diabetic nerves. This article summarizes experimental data indicating that a dysfunction of ion conductances, especially voltage-gated ion channels, could contribute to abnormalities in the generation and/or conduction of action potentials in diabetic neuropathy.
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