Intrathecal magnesium sulfate attenuates algogenic behavior and spinal amino acids release after kainic acid receptor activation in rats.

Activation of N-methyl-D-asparate (NMDA) receptor and non-NMDA classes of glutamate receptors play a key role in spinal nociceptive processing. Using with a lumbar intrathecal (IT) catheter and a loop dialysis catheter in lightly anesthetized (1% isoflurane) rats, the effect of IT pre-treatment with magnesium sulfate (100, 300 or 500 microg) on IT kainic acid (KA: 1 microg; non-NMDA receptor agonist) evoked amino acids (AAs) release and corresponding behavior was examined. IT KA produced significant increases (mean+/-SD of % baseline concentration) in dialysate concentrations of aspartate (424+/-88%), glutamate (241+/-35%) and taurine (398+/-58%). IT pre-treatment with MgSO(4) resulted in a dose-dependent suppression of the evoked algogenic behavior and aspartate release. These data suggest that activation of spinal KA receptors provides a powerful stimulus for secondary spinal excitatory AAs release and corresponding appearance of pain behavior. The regulation of this release by magnesium suggests the possible role of this divalent cation in regulating this excitatory effect of non-NMDA receptor activation.