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Epinephrine and norepinephrine modulate neuronal responses to excitatory amino acids and agonists in frog spinal cord
Author(s) -
Wohlberg C. J.,
Hackman J. C.,
Davidoff R. A.
Publication year - 1987
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890010208
Subject(s) - excitatory postsynaptic potential , chemistry , glutamate receptor , nmda receptor , yohimbine , agonist , medicine , norepinephrine , endocrinology , neurotransmission , neuroscience , pharmacology , receptor , dopamine , antagonist , biology , biochemistry
The interaction of catecholamines epinephrine (E) and norepinephrine (NE) (1.0–100 μM) 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 ne β‐adrenoceptor mediated because it was mimicked by the β‐agonist isoprotereno and blocked by propranolol. The effect on quisqualate depolarizations appeared to require activation of α 2 ‐adrenoceptors; it was mimicked by the α 2 ‐agonists clonidine and α‐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.