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°C), myelin-deficient rats had longer cortical SEP latencies (67 ± 20 ms) compared to those in normal siblings (48 ± 15 ms; P < 0.05). Mean baseline [K +] e levels were 2.6 ± 0.5 m M in myelin-deficient rats and 2.6 ± 0.8 m M 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 m M 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 μm depth. The normal siblings had smaller or no stimulus-induced [K +] e rises. In myelindeficient rats, injection of 1 m M 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.