title: Extracellular potassium activity and axonal conduction in spinal cord of the myelin-deficient mutant rat.
abstract: We recorded somatosensory evoked potentials SEPs), extracellular K+ ionic activity ([K+]e), and K+ clearance rates in the spinal cords of 14 myelin-deficient mutant rats and 16 normal male littermates at 16-41 days after birth. Tested under pentobarbital anesthesia (25 mg/kg ip) and hypothermic conditions (32-34 degrees C), myelin-deficient rats had longer cortical SEP latencies (67 +/- 20 ms) compared to those in normal siblings (48 +/- 15 ms; P less than 0.05). Mean baseline [K+]e levels were 2.6 +/- 0.5 mM in myelin-deficient rats and 2.6 +/- 0.8 mM in normal siblings. Clearance times of KCl solutions injected into the spinal cord were biphasic and exponential. The mean initial and secondary exponential half-times were 1.0 +/- 0.5 and 2.7 +/- 1.7 min for myelin-deficient rats and 0.8 +/- 0.4 and 3.8 +/- 3.2 min for normal siblings. Repetitive sciatic nerve stimulation (2-20 Hz, 2- to 6-s trains) produced 1-3 mM transient [K+]e rises in thoracic and lumbar cords of myelin-deficient rats. The [K+]e rises were largest in the dorsal spinal cord at 200-500 microns depth. The normal siblings had smaller or no stimulus-induced [K+]e rises. In myelin-deficient rats, injection of 1 mM 4-aminopyridine (4-AP) solution into the thoracic spinal cord completely suppressed the stimulus-induced [K+]e and markedly increased spinal and cortical SEP amplitudes for several hours. In the normal siblings, the 4-AP injections transiently blocked spinal conduction for 20-30 min but thereafter enhanced cortical SEP amplitudes for 2-3 h. We conclude that sciatic nerve stimulation produces spinal cord [K+]e rises in myelin-deficient rat larger than those in the normal siblings, that the [K+]e transients represent increased K+ release rather than impaired K+ clearance, and that the K+ ions come from 4-AP blockable sources.
authors.affiliation: Department of Neurosurgery, New York University School of Medicine, New York.
authors.forename: W
authors.initials: W
authors.lastname: Young
authors.forename: J
authors.initials: J
authors.lastname: Rosenbluth
authors.forename: J C
authors.initials: JC
authors.lastname: Wojak
authors.forename: K
authors.initials: K
authors.lastname: Sakatani
authors.forename: H
authors.initials: H
authors.lastname: Kim
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D001369:Axons / Q000502:physiology* / Q000648:ultrastructure; D004553:Electric Conductivity; D004558:Electric Stimulation; D005071:Evoked Potentials; D008297:Male; D008854:Microscopy, Electron; D009186:Myelin Sheath / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D011189:Potassium Chloride / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012584:Sciatic Nerve / Q000502:physiology; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure
chemical_list: D011189:Potassium Chloride; D015761:4-Aminopyridine; D011188:Potassium