SPINAL-CORD ISCHEMIA-INDUCED EXCITOTOXICITY AND NEURODEGENERATION - ATTENUATION BY (-)-DEPRENYL AND MAGNESIUM-SULFATE

We have evaluated the neuroprotective role of (-) deprenyl, a selectiv e monoamine oxidase-B (MAO-B) inhibitor, and magnesium sulfate (MgSO4) , a non-competitive N-methyl-D-aspartate (NMDA) receptor blocker, on i schaemia-induced excitotoxicity. Spinal cord ischaemia was induced tra nsiently in freely moving conscious rats by a modified snare ligature. The drugs were administered post-ischaemically to different groups of rats for 14 days. The levels of glutamate were significantly (P < 0.0 01) higher in the ischaemized group. However, the normal levels of glu tamate persisted in animals treated with (-) deprenyl or MgSO4. In add ition, qualitative examination of spinal motor neurons at the lumbar l evel showed degenerated neurons in the ischaemized and vehicle-treated groups of rats. Treatment with (-) deprenyl or MgSO4 protected the mo tor neurons from degeneration. Our findings suggest that postischaemic administration of (-) deprenyl or MgSO4 attenuates the glutamate-indu ced excitotoxicity and reduces the degeneration of spinal cord motor n eurons. Further, (-) deprenyl and MgSO4 can have neuroprotective effec ts through the regulation of glutamate-induced excitotoxicity. (C) 199 8 Chapman & Hall Ltd.