Abstract
The peripheral administration of morphine1–4 or the intraventricular injection of either Met-enkephalin or D-Ala2-Met-enkephalinamide4 (a synthetic enkephalin analogue resistant to enzyme degradation) enhanced dopamine (DA) turnover in the rat striatum. These effects, in turn, could be blocked by the opiate antagonist naloxone1,4. As the striatum contains a high density of opiate receptors5, these drugs may be affecting DA metabolism by a local action. This hypothesis is supported by the evidence that morphine still enhanced striatal DA turnover shortly after transection of the nigro-striatal DA pathway6. Furthermore, D-Ala2-Met-enkephalinamide directly injected into the striatum significantly increased striatal DA turnover4. However, the mechanism by which opiates stimulate DA turnover is not clear because they have not yet been shown to enhance DA outflow in in vitro release studies7–9. We have therefore now examined in vivo the local effects of opiates on the release of DA in the cat caudate nucleus. We find that both morphine and more markedly, D-Ala2-Met-enkephalinamide stimulate DA release. The action of morphine is antagonized by naloxone, but that of the synthetic enkephalin is not. Because the effects of D-Ala2-Met-enkephalinamide are similar to those of the peripheral δ-receptor agonist Tyr-D-Ser-Gly-Phe-Leu-Thr, we conclude that the synthetic enkephalin acts on δ-receptors.
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Chesselet, M., Chéramy, A., Reisine, T. et al. Morphine and δ-opiate agonists locally stimulate in vivo dopamine release in cat caudate nucleus. Nature 291, 320–322 (1981). https://doi.org/10.1038/291320a0
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DOI: https://doi.org/10.1038/291320a0
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