Abstract. An analysis of the role of adrenergic transmission in mediating the hyperpolarizing, slow inhibitory postsynaptic potential has revealed that dopamine is apparently the specific synaptic transmitter for this response. An additional action of dopamine was discovered, namely the selective facilitation of another synaptic response, the slow excitatory postsynaptic potential. (This potential is a depolarizing response to the muscarinic action of acetylcholine.) This second,,,modulatory, role of dopamine has characteristics strikingly different from other known modes of synaptic action. After a brief initial action by dopamine, the facilitation of the slow excitatory postsynaptic potential response can persist for hours and is unaffected by a delayed blockade of the postsynaptic receptors for dopamine. This suggests that the modulation consists of a long-lasting metabolic and/or structural change induced in the postsynaptic neuron by dopamine.These conclusions are based on the demonstrated actions of dopamine and other catecholamines, as well as on effects (on dopamine actions and on slow postsynaptic potentials of alpha-adrenergic blockers, of blockade, of dopamine oxidase, of depletion of ganglionic catecholamine by muscarinic excitation, and of a selective re-uptake of dopamine after such depletion.Sympathetic ganglia respond to preganglionic impulses with two slow postsynaptic potentials (PSPs) that have synaptic delays in the tens and hundreds of msec and durations in the tens of seconds.' 3 The mechanisms of electrogenesis of both of the slow PSPs do not involve increases in ionic conductance of the membrane.4 Their synaptic mediation also differs from that of the well-known fast (excitatory) postsynaptic potential (EPSP). The slow excitatory response (S-EPSP) is elicited by a muscarinic, instead of a nicotinic action, of acetylcholine (ACh).2'5 The slow inhibitory response (S-IPSP) also involves a muscarinic action by the ACh released from preganglionic terminals; but the evidence strongly supports the hypothesis that this cholinergic action is on an adrenergic interneuron and brings about the release of catecholamine.2'6 This catecholamine then directly elicits the hyperpolarizing S-JPSP of the ganglion cell. We now present evidence that the specific catecholamine acting as adrenergic transmitter for the S-IPSP is dopamine (3,4-dihydroxyphenylethyl-667
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