Inhibition of spinal monosynaptic reflex in newborn rats by aurintricarboxylic acid.

The effect of aurintricarboxylic acid (ATA), an inhibitor of nuclease, on glutamatergic synaptic transmission was examined electrophysiologically in the isolated spinal cords of newborn rats. Monosynaptic reflex (MSR) was depressed about 20%, 50 min after exposure to 100 microM of ATA. Pretreatment with APV, a N-methyl-D-aspartate (NMDA) type receptor antagonist, depressed MSR by about 10%, but additional application of ATA did not affect the MSR further. In contrast, the remaining MSR following treatment with DNQX, a non-NMDA type receptor antagonist, in the Mg2+-free medium was almost completely inhibited by addition of ATA. ATA depressed NMDA- but not D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic acid (AMPA)- or kainate-induced depolarization in the medium containing normal ionic composition. Thus it is concluded that the reduction of MSR by ATA is due to blockade of NMDA type but non-NMDA type glutamate receptors. The present study also confirmed the previous conclusion that Ia monosynaptic transmission in the spinal cord of the newborn rat is mediated by NMDA as well as non-NMDA type glutamate receptors.