A NEW MODEL OF ACUTE COMPRESSIVE SPINAL-CORD INJURY IN-VITRO

A novel in vitro method of spinal cord injury was developed to facilit ate the study of cellular and molecular mechanisms underlying neural t rauma. A 3-cm length of thoracic spinal cord was removed from the adul t Wistar rat. A strip of dorsal column and its associated dorsal horn gray matter was excised and pinned in an in vitro recording chamber wh ere it was constantly perfused with oxygenated Ringer's solution at ei ther 25 degrees C or 33 degrees C. Injury was performed by compressing the dorsal column segment in vitro with a modified aneurysm clip (clo sing force 2.0 g) for 15 s. Microelectrode and sucrose gap recordings were generated to characterize the physiological effects of compressiv e injury. Longitudinal thin sections of control and injured dorsal col umn segments were examined by electron microscopy. At 25 degrees C, in jured axons were characterized by a significant reduction in amplitude of the compound action potential (CAP) to 76.9 +/- 2.4% (P<0.0005) an d an increase in response latency to 112.5 +/- 2.5% (P < 0.005). At 33 degrees C, the effects of injury on the CAP amplitude were accentuate d (P < 0.0001). With the K+ channel blocker, 4-AP (1 mM), there was br oadening of the CAP of injured axons and a delay in repolarization of the axonal resting membrane potential, suggesting myelin disruption wi th exposure of paranodal K+ channels. Ultrastructurally, injured dorsa l column segments showed considerable axonal and myelin pathology incl uding splaying of the myelin sheath and vesicular degeneration. (C) 19 97 Elsevier Science B.V.