Abstract
The endogenous opioid peptides, enkephalins, are known to be concentrated in discrete populations of central and peripheral neurones1–3 and to inhibit synaptic transmission through a presynaptic mechanism reducing the release of transmitters4–6. These observations led to a hypothesis that enkephalin may serve as a transmitter for presynaptic inhibition at central and peripheral synapses4,5. To substantiate this hypothesis it is of crucial importance to demonstrate at specified synapses an inhibitory process that is evoked by stimulation of enkephalin-containing nerve fibres and is blocked by the opiate antagonist, naloxone. Mammalian sympathetic ganglia may provide a useful model for exploring this possibility, because enkephalin was shown, using immunohistochemistry3, to exist in certain nerve terminals in the ganglia and to inhibit cholinergic and noncholinergic transmission by a presynaptic mechanism5,7,8. We now report that in mammalian prevertebral ganglia, the conditioning stimulation given to preganglionic nerves produces a long-lasting presynaptic inhibition of cholinergic transmission and that this inhibition is specifically abolished by naloxone. The results strongly suggest that enkephalin or closely related peptide(s) liberated from certain preganglionic fibres act as a transmitter for presynaptic inhibition, regulating the release of acetylcholine (ACh) in the sympathetic ganglia.
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Konishi, S., Tsunoo, A. & Otsuka, M. Enkephalin as a transmitter for presynaptic inhibition in sympathetic ganglia. Nature 294, 80–82 (1981). https://doi.org/10.1038/294080a0
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DOI: https://doi.org/10.1038/294080a0
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