Changes in electrophysiological properties of regenerating rat peripheral nerves after crush injury

• Published in: Neuroscience letters 2004-06, Vol.363 (3), p.212-217
• Main Authors: Mert, Tufan, Daglioglu, Yusuf Kenan, Gunay, Ismail, Gocmen, Cemil
• Format: Article
• Language: English
• Subjects: 4-Aminopyridine; 4-Aminopyridine - pharmacology; Action Potentials - drug effects; Action Potentials - physiology; Animals; Biological and medical sciences; Crush injury; Delayed depolarization; Electric Stimulation; Electrophysiology - methods; Female; Fundamental and applied biological sciences. Psychology; Lidocaine; Lidocaine - pharmacology; Nerve Crush - methods; Nerve Regeneration - physiology; Neural Conduction - drug effects; Neural Conduction - physiology; Peripheral Nerves - physiology; Potassium Channel Blockers - pharmacology; Rats; Regeneration; Sciatic Neuropathy - physiopathology; Sodium Channel Blockers - pharmacology; Tetraethylammonium - pharmacology; Time Factors; Vertebrates: nervous system and sense organs; Wounds and Injuries - physiopathology
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2004.03.018

The conduction of action potential in peripheral nerves requires the coordinated opening and closing of Na + and K + channels. In the present study, we used the sucrose-gap recording technique to determine the electrophysiological changes of the regenerating nerves after sciatic nerve injury by using 4-aminopyridine (4-AP) and tetraethylammonium (TEA), and lidocaine. 4-AP enhanced the amplitude and duration of the compound action potentials (CAPs) of regenerating sciatic nerve 15 days post crush (15 dpc), and elicited delayed depolarizations (Del-dep) in 38 dpc and intact groups. Hyperpolarizing afterpotentials elicited by 4-AP were completely removed by TEA in both 15 and 38 dpc. Lidocaine effectively blocked the CAP amplitude. This blockage was more pronounced in 15 dpc than 38 dpc. This agent also exhibited a partial blockage on the Del-dep amplitude. These results may indicate that the changes in the activities of 4-AP- and TEA-sensitive K + channels and slow Na + channels may play critical roles in nerve excitability and conduction.