The interaction of the catecholamines epinephrine (E) and norepinephrine (NE) (1.0-100 microM) and excitatory amino acids on motoneurons of the isolated superfused frog spinal cord was investigated by sucrose gap recordings from ventral roots. Exposure of the cord to E or NE 30 sec prior to application of L-aspartate or L-glutamate reduced the motoneuron depolarizations produced by the amino acids. The reduction of responses to the mixed receptor agonists L-glutamate and L-aspartate may be the result of opposite actions of the catecholamines on the activation of specific excitatory receptors by the amino acids. Thus, E and NE facilitated depolarizations caused by application of N-methyl-D-aspartate (NMDA) and depressed those produced by quisqualate. The effect on NMDA responses appeared to be beta-adrenoceptor mediated because it was mimicked by the beta-agonist isoproterenol and blocked by propranolol. The effect on quisqualate depolarizations appeared to require activation of alpha 2-adrenoceptors; it was mimicked by the alpha 2-agonists clonidine and alpha-methylnorepinephrine and antagonized by yohimbine and piperoxan. These results are important in understanding the actions of catecholamines on reflex transmission in spinal pathways which use excitatory amino acids as transmitters.