@entity409 in an in vitro model of acute compressive injury to adult XXXX spinal cord axons.

@entity1 @entity35 @entity973 @entity409 @entity515 @entity974 @entity439 @entity1566 @entity130
An in vitro model of @entity1566 was developed to study the pathophysiology of posttraumatic @entity409 . A 25 mm length of thoracic spinal cord was removed from the adult male @entity35 (n = 27). A dorsal column segment was isolated and pinned in a recording chamber and superfused with oxygenated (95% O2/5% @entity515 ) Ringer. The cord was stimulated with a bipolar electrode, while two point responses were recorded extracellularly. Injury was accomplished by compression with a modified @entity439 which applied a 2 g force for 15 s. With injury the compound action potential (CAP) amplitude decreased to 53.7 +/- 5.4% (P < 0.001), while the latency increased to 115.6 +/- 3.1% (P < 0.0025) of control values. The absolute refractory period increased with injury from 1.7 +/- 0.1 ms to 2.1 +/- 0.1 ms (P < 0.05). The infusion of 5 mM @entity973 ( @entity974 ), a blocker of voltage-sensitive 'fast' K channels confined to internodal regions, resulted in broadening of the CAP of injured axons to 114.9 +/- 3.1% of control (P < 0.05). Ultrastructural analysis of the injured dorsal column segments revealed marked axonal and myelin pathology, including considerable myelin disruption. In conclusion, we have developed and characterized an in vitro model of @entity1 @entity1566 which simulates many of the features of in vivo @entity130 . Injured axons display characteristic changes in physiological function including a shift in refractory period and high frequency conduction failure. The ultrastructural data and response of injured axons to 4-AP suggest that myelin disruption with exposure of 'fast' K+ channels contributes to posttraumatic @entity409 .
