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. 1970 Oct;67(2):667-73.
doi: 10.1073/pnas.67.2.667.

Dopamine as a synaptic transmitter and modulator in sympathetic ganglia: a different mode of synaptic action

Dopamine as a synaptic transmitter and modulator in sympathetic ganglia: a different mode of synaptic action

B Libet et al. Proc Natl Acad Sci U S A. 1970 Oct.

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.

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References

    1. J Pharm Pharmacol. 1965 Aug;17(8):526-7 - PubMed
    1. J Neurophysiol. 1967 May;30(3):494-514 - PubMed
    1. Proc Natl Acad Sci U S A. 1968 Aug;60(4):1304-11 - PubMed
    1. J Neurophysiol. 1969 Jan;32(1):43-50 - PubMed
    1. J Ultrastruct Res. 1968 Dec;25(5):381-407 - PubMed

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