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Met-enkephalin inhibits 5-hydroxytryptamine release from the rat ventral spinal cord via delta opioid receptors
Department of Clinical Neuroscience, Alcohol and Drug Dependence Research Section, Karolinska Hospital. (Pharmacology)
1996 (English)In: Neuropharmacology, ISSN 0028-3908, E-ISSN 1873-7064, Vol. 35, no 6, 743-749 p.Article in journal (Refereed) Published
Abstract [en]

The effect of opioid receptor agonists and antagonists on the electrically evoked release of endogenous serotonin (5-hydroxytryptamine, 5-HT) was studied in superfused slices of the rat ventral lumbar spinal cord. Met-ENK (1 x 10(-8)M-1 x 10(-6)M) and DPDPE (1 x 10(-8)M-1 x 10(-6)M) reduced the evoked 5-Ht release in a concentration dependent fashion. DAMGO (1 x 10(-8)-1 x 10(-6)) and (-)-trans-(1S,2S)-U-50488 (1 x 10(-6)M) had no effect on the 5-HT release. The inhibitory effect of met-ENK was completely abolished by ICI-174,864, but neither by naloxonazine nor nor-binaltorphimine. Following i.c.v. treatment with 5,7-dihydroxytryptamine (5,7-DHT), the tissue concentration of 5-HT was reduced by 97%, whereas the concentration of noradrenaline was reduced by only 5%. The tissue concentration of met-ENK, as measured by radioimmunoassay, was not significantly altered. The results suggest that met-ENK is present in the rat ventral spinal cord mainly in non-serotonergic nerve terminals and exerts an inhibitory action on 5-HT release via delta opioid receptors.

Place, publisher, year, edition, pages
1996. Vol. 35, no 6, 743-749 p.
Keyword [en]
DAMGO, DPDPE, 5, 7-dihydroxytryptamine, 5-hydroxytryptamine, ICI-174, 864, met-enkephalin, naloxonazine, nor-binaltorphimine, opioid receptors, spinal cord slices (ventral), (-)-trans-(1S, 2S)-U-50488
National Category
Pharmaceutical Sciences Medical and Health Sciences
URN: urn:nbn:se:uu:diva-51073DOI: 10.1016/0028-3908(96)84646-6ISI: A1996VK79300012PubMedID: 8887983OAI: oai:DiVA.org:uu-51073DiVA: diva2:78982
Available from: 2008-10-17 Created: 2008-10-17 Last updated: 2011-03-09Bibliographically approved

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