The interaction of the catecholamines epinephrine (E) and norepinephrine (NE) (1.0-100 pM) 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 P-adrenoceptor mediated because it was mimicked by the 8-agonist isoproterenol and blocked by propranolol. The effect on quisqualate depolarizations appeared to require activation of a2-adrenoceptors; it was mimicked by the cr2agonists clonidine and a-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.
cord and can affect the excitability of afferent terminals Available data show that catecholamine-containing fi-@Yan et a]-, 1983; Wohlberg et al., 1985b), interneurons bers originating in the mammalian brain stem termi- (Engberg and &all, 1966;Ryan et al., 1984), and motonate in the spinal gray matter in the vicinity of neurons Marshall and Engberg, 1979; VanderMaelen interneurons and motoneurons (Marshall, 1983). Norepi-and AghaJanian, 1980;White and Neuman, 1980; Wohlnephrine (NE) released from the terminals of these de-berg et al-, 1984) in ways which could both increase and scending bulbospinal fibers presumably activates decrease reflex transmission. In addition, there are conadrenoceptors located on neurons in both the dorsal and flicting reports that catecholamines both hyperpolarize ventral horns (