Increased spike-frequency adaptation and tea sensitivity in dorsal root fibers after sciatic nerve injury.
Excitability of rat dorsal root axons were studied 3 weeks after injury to the sciatic nerve. Whole nerve recordings were obtained from injured and control nerves in a sucrose gap chamber. Constant current depolarization pulses (30-200 ms) applied approximately 50% above the stimulus strength required for maximal amplitude compound action potentials (CAPs) evoked a burst of action potentials in the dorsal root which displayed spike adaptation. The depolarization-induced burst response of the dorsal roots was greatly reduced after crush or transection of the sciatic nerve. However, application of the potassium channel blocker, tetraethylammonium (TEA), restored the burst discharge in injured dorsal root axons. Brief tetanic stimulation of the dorsal root also induced an afterhyperpolarization (AHP) that was twice as large in the transection group as compared to the control group, and which was blocked by TEA. There were no changes seen in the amplitude of the compound action potential, frequency-following characteristics, refractory properties, or 4-AP sensitivity in the dorsal roots after peripheral nerve injury. These results suggest that there is enhanced spike adaptation that occurs at the same time as an increase in the sensitivity to the potassium channel blocker, TEA, in axon regions proximal to the site of nerve injury and have implications for the pathophysiology of nerve injury.
Utzschneider
D A
DA
Department of Neurology, Yale University School of Medicine, New Haven, Connecticut.
Bhisitkhul
R B
RB
Kocsis
J D
JD
D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials; D000222:Adaptation, Physiological; D000818:Animals; D004558:Electric Stimulation; D004594:Electrophysiology; D005260:Female; D009412:Nerve Fibers / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012584:Sciatic Nerve / Q000293:injuries*; D013126:Spinal Nerve Roots / Q000187:drug effects* / Q000503:physiopathology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology*; D014947:Wounds and Injuries / Q000503:physiopathology
D013757:Tetraethylammonium Compounds; D019789:Tetraethylammonium; D015761:4-Aminopyridine