BACKGROUND The demyelination process has been proven to be an importan
t factor contributing to long-term sensory and motor impairments after
spinal cord injury (SCI). The loss of myelin promotes exposure of Kchannels in internodal region of the damaged myelinated axons leading
to KC efflux into the neurons with subsequent blockage of action poten
tials. The potassium channel blocker 4-aminopyridine (4-AP) has been e
ffective in restoring some sensory and motor impairment in incomplete
SCI patients, The effect of this compound given immediately after an a
cute injury is not known. The objective of this study was to determine
if blockage of K+ ions efflux immediately after an acute SCI would im
prove neuronal conduction in this model of injury. METHODS Cortical so
matosensory evoked potentials (SSEPs) were recorded before and after a
weight-induced compression injury of 120 grams, and were monitored up
to 5 hours postinjury. A randomized treatment was initiated with admi
nistration of either vehicle or 4-AP. All 4-AP treatments were given a
s intravenous bolus injections of 1.0, 0.5, and 0.3 mg/kg at 1, 2, and
3 hours after the trauma. RESULTS The SSEPs were abolished immediatel
y after the injury in all control and treated animals, Both groups sho
wed spontaneous recovery of the SSEPs at the rate of 44.5% for the 4-A
P treated and nontreated groups at the second hour postinjury, This re
covery rate remained the same for both groups at the end of the experi
ments. CONCLUSIONS Based on the recovery of the SSEPs, our data indica
te that early administration of 4-AP lacks any beneficial effect on ax
onal function during acute stage of spinal cord injury.