Involvement of protein kinase C in the nitric oxide-mediated peripheral nerve disturbance in endotoxemic rats

The role of protein kinase C (PKC) in nitric oxide (NO)-mediated peripheral nerve disturbance in lipopolysaccharide (endotoxin, LPS)-treated rat was studied. The impaired Na+,K+-ATPase activities in sciatic nerves from LPS-treated rats were prevented by aminoguanidine (NO synthase inhibitor) and cor...

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Bibliographic Details
Published in:Neuroscience letters 1999-01, Vol.259 (2), p.99-102
Main Authors: Liu, Shing H, Wang, Jei H, Fang, Kuang T, Lin-Shiau, Shoei Y
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Endotoxemia - pathology
Fundamental and applied biological sciences. Psychology
Lipopolysaccharides - pharmacology
Male
Na+,K+-ATPase
Nitric oxide
Nitric Oxide - physiology
Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ
Protein kinase C
Protein Kinase C - metabolism
Protein Kinase C - physiology
Rats
Rats, Wistar
Sciatic nerve
Sciatic Nerve - drug effects
Sciatic Nerve - physiology
Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors
Vertebrates: nervous system and sense organs
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Summary:The role of protein kinase C (PKC) in nitric oxide (NO)-mediated peripheral nerve disturbance in lipopolysaccharide (endotoxin, LPS)-treated rat was studied. The impaired Na+,K+-ATPase activities in sciatic nerves from LPS-treated rats were prevented by aminoguanidine (NO synthase inhibitor) and corrected by PKC agonist in vitro. Using Western blot to determine PKC isoforms α and β polypeptide levels in LPS-treated rat sciatic nerves, we found that α isoform was markedly reduced in the particulate fraction, but the β isoform was unaffected. The α and β isoforms in the cytosolic fractions were not significantly different as compared with control. This diminished particulate PKC α isoform was prevented by the treatment of aminoguanidine. Moreover, the motor nerve conduction velocity was significantly reduced in endotoxemic rats and corrected by aminoguanidine. These results indicate that the alteration of PKC α isoform in Na+,K+-ATPase-enriched fraction of sciatic nerve may be related to the NO-mediated peripheral nerve disturbance in endotoxemic rats.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(98)00910-0