MK 801, an OBS N-methyl-D-aspartate channel blocker, does not improve the functional recovery nor spinal cord blood flow after spinal cord compression in rats

Abstract

Damage to the central nervous system is followed by local release of excitatory amino acids, e.g. glutamate. These have been claimed to increase the metabolic need of already hypoxic neurons, and thereby to promote cell death. To investigate whether N-methyl-D-aspartate (NMDA) receptor-mediated mechanisms are involved in the damage consequent to spinal cord injury, 20 rats were exposed to 5-min compression of the thoracic spinal cord produced with a load of 35 g on a 2.2 x 5 mm sized plate. One group of animals was given a noncompetitive NMDA channel blocker, MK-801, in a dose of 10 mg/kg b.w and one group saline alone. The neurologic function was evaluated on the inclined plane for 4 days when spinal cord blood flow (SCBF) was measured with the 14C-iodoantipyrine autoradiographic technique. One day after trauma the animals in both groups were paraparetic and exhibited a significantly decreased capacity angle at the inclined plane test (about 35 degrees compared with about 63 degrees before compression). Thereafter, the motor function improved slightly, but to a similar extent in the two groups. On Day 4, gray and white matter SCBF was similar in the two groups. The results indicate that MK 801 in the dose used does not prevent the development of neurologic dysfunction or the reduction in SCBF after spinal cord compression.