Nerve compression induces activating transcription factor 3 in neurons and Schwann cells in diabetic rats.
ABSTRACT Expression of transcription factor ATF3 in sensory neurons in dorsal root ganglion and in Schwann cells in sciatic nerve of diabetic (BB and Goto-Kakizaki rats; experimental models of types 1 and 2 diabetes, respectively) and healthy rats were examined by immunocytochemistry after nerve compression (silicone tube) for 3, 6 or 14 days. ATF3-stained sensory neurons in dorsal root ganglia and Schwann cells at compression site were more frequent in diabetic BB rats. Decompression of nerves in Goto-Kakizaki rats did not reduce number of ATF3-stained cells. Diabetes (BB; i.e. type 1) confers on the peripheral nerve an increased susceptibility to nerve compression indicated by an increased expression of stained ATF3 neurons and Schwann cells.
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ABSTRACT: Prolonged exposure to hand-held vibrating tools may cause a hand-arm vibration syndrome (HAVS), sometimes with individual susceptibility. The neurological symptoms seen in HAVS are similar to symptoms seen in patients with carpal tunnel syndrome (CTS) and there is a strong relationship between CTS and the use of vibrating tools. Vibration exposure to the hand is known to induce demyelination of nerve fibres and to reduce the density of myelinated nerve fibres in the nerve trunks. In view of current knowledge regarding the clinical effects of low nerve-fibre density in patients with neuropathies of varying aetiologies, such as diabetes, and that such a low density may lead to nerve entrapment symptoms, a reduction in myelinated nerve fibres may be a key factor behind the symptoms also seen in patients with HAVS and CTS. Furthermore, a reduced nerve-fibre density may result in a changed afferent signal pattern, resulting in turn in alterations in the brain, further prompting the symptoms seen in patients with HAVS and CTS. We conclude that a low nerve-fibre density lead to symptoms associated with nerve entrapment, such as CTS, in some patients with HAVS.Journal of Occupational Medicine and Toxicology 03/2014; 9(1):7.
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ABSTRACT: In view of the global increase in diabetes, and the fact that recent findings indicate that diabetic neuropathy is more frequently seen in males, it is crucial to evaluate any gender differences in nerve regeneration in diabetes. Our aim was to evaluate in short-term experiments gender dissimilarities in axonal outgrowth in healthy and in genetically developed type 2 diabetic Goto-Kakizaki (GK) rats, and also to investigate the connection between activated (i.e. ATF-3, Activating Transcription Factor 3) and apoptotic (cleaved caspase 3) Schwann cells after sciatic nerve injury and repair. Female and male diabetic GK rats, spontaneously developing type 2 diabetes, were compared with corresponding healthy Wistar rats. The sciatic nerve was transected and instantly repaired. After six days the nerve was harvested to measure axonal outgrowth (i.e. neurofilament staining), and to quantify the number of ATF-3 (i.e. activated) and cleaved caspase 3 (i.e. apoptotic) stained Schwann cells using immunohistochemistry.BMC Neuroscience 09/2014; 15(1):107. · 3.00 Impact Factor
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ABSTRACT: Significance: Mitochondrial dynamics describes the continuous change of position, size and shape of mitochondria within cells. The morphological and functional complexity of neurons, the remarkable length of their processes and the rapid changes in metabolic requirements arising from their intrinsic excitability, render these cells particularly dependent on effective mitochondrial function and positioning. The rules which govern these changes and their functional significance are not fully understood, yet the dysfunction of mitochondrial dynamics has been implicated as a pathogenetic factor in a number of diseases, including disorders of central and peripheral nervous systems. Recent advances: In recent years, a number of mutations of genes encoding proteins which play important roles in mitochondrial dynamics and function have been discovered in patients with Charcot-Marie-Tooth (CMT) disease, a hereditary peripheral neuropathy. These findings have directly linked mitochondrial pathology to the pathology of peripheral nerve and have identified certain aspects of mitochondrial dynamics as potential early events in the pathogenesis of CMT. In addition, mitochondrial dysfunction has now been implicated in the pathogenesis of non-inherited neuropathies, including diabetic and inflammatory neuropathies. Critical issues: The role of mitochondria in peripheral nerve diseases has been mostly examined in vitro, and less so in animal models. Future directions: This review examines available evidence for the role of mitochondrial dynamics in the pathogenesis of peripheral neuropathies, their relevance to human diseases and future challenges for research in this field.Antioxidants & Redox Signaling 01/2014; · 8.20 Impact Factor