Premium
Ethanol‐Induced Increase in Endogenous Dopamine Release May Involve Endogenous Opiates
Author(s) -
Widdowson Peter S.,
Holman R. Bruce
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb08886.x
Subject(s) - enkephalin , chemistry , medicine , endocrinology , dadle , (+) naloxone , agonist , opioid peptide , endogeny , endogenous opioid , opiate , stimulation , opioid receptor , antagonist , opioid , receptor , biology , biochemistry
The effect of opiate peptides on basal and potassium‐stimulated endogenous dopamine (DA) release from striatal slices was studied in vitro. Dual stimulation of the striatal slices gave a reproducible increase in DA release that was calcium dependent. Addition of the δ‐opiate receptor agonists Met 5 ‐enkephalin, [D‐Ala 2 ,D‐Leu 5 ]enkephalin (DADLE), and [D‐Ser]Leu‐enkephalin‐Thr (DSLET), increased the basal DA release without affecting potassium‐stimulated release in a dose‐dependent manner. The effect of DADLE was antagonized by the addition of naloxone. In contrast, the μ‐opioid receptor agonist [D‐Ala 2 , N ‐MePhe 4 ,Gly‐ol 5 ]enkephalin (DAGO) and the e ‐opioid agonist β‐endorphin inhibited the stimulated DA release without changing the basal release. The inhibitory effect of DAGO on potassium‐stimulated release was antagonized by naloxone. The addition of ethanol (75 m M ) to the incubation media produced a delayed increase of both the basal and stimulated DA release. There was no change in stimulated DA release when the change in basal release was subtracted, suggesting that ethanol produced a dose‐dependent, selective increase in basal DA release. Naloxone and the selective δ‐opiate antagonist ICI 174864 inhibited the eth‐anol‐induced increase in basal DA release. Naloxone and ICI 174864 added alone did not alter either basal or stimulated DA release. We therefore suggest that the ethanol‐in‐duced increase in basal DA release is an indirect effect involving an endogenous δ‐opiate agonist.