β-Endorphin in vitro inhibition of striatal dopamine release

Loh, Horace H.; Brase, David A.; Sampath-Khanna, Sumathy; Mar, Jeffrey B.; Way, E. Leong; Li, Choh Hao

doi:10.1038/264567a0

Cited by 256 publications

(41 citation statements)

References 15 publications

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“…Some previous studies showed that acute systemic administration of opioids did not increase the release of nigrostriatal DA (Ahtee et al, 1989;Wood & Rao, 1991;Wood & Richard, 1982;Wood et al, 1980;Yonehara & Clouet, 1984). Also, in studies in which DA release was measured from striatal slices, it has been shown that m-opioids somewhat retard the release of DA (Celsen & Kuschinsky, 1974;Kuschinsky et al, 1975;Loh et al, 1976;Schlosser et al, 1995;Widdowson & Holman, 1992). The results of the present study con®rm that there is an inhibitory, naltrexone-sensitive component in the e ect of opioids on striatal DA release.…”

Section: Discussionsupporting

confidence: 72%

Characterization of the decrease of extracellular striatal dopamine induced by intrastriatal morphine administration

Piepponen

Mikkola

Ruotsalainen

et al. 1999

British J Pharmacology

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1 The e ect of intrastriatally-administered morphine on striatal dopamine (DA) release was studied in freely moving rats. Morphine (1, 10 or 100 mM) was given into the striatum by reversed microdialysis, and concentrations of DA and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were simultaneously measured from the striatal dialysates. 2 Intrastriatally-administered morphine signi®cantly and dose-dependently decreased the extracellular concentration of DA, the concentrations of the acidic DA metabolites were only slightly decreased. The e ect of morphine was antagonized by naltrexone (2.25 mg kg 71 , s.c.). Pretreatment with a preferential k-opioid receptor antagonist, MR2266 [(7)-5,9 alpha-diethyl-2-(3-furylmethyl)-2'-hydroxy-6,7-benzomorphane; 1 mg kg 71 , s.c.], had no e ect on the decrease of extracellular DA evoked by intrastriatal morphine (100 mM). 3 Intrastriatal administration of the selective m-opioid receptor agonist [D-Ala 2 ,MePhe 4 ,Gly-ol 5 ] enkephalin (DAMGO; 1 mM), signi®cantly decreased the extracellular concentration of DA in the striatum. 4 When the rats were given morphine repeatedly in increasing doses (10 ± 25 mg kg 71 , s.c.) twice daily for 7 days and withdrawn for 48 h, the decrease of extracellular DA induced by morphine (100 mM) was signi®cantly less than that seen in saline-treated controls. 5 Our results show that besides the well-known stimulatory e ect there is a local inhibitory component in the action of morphine on striatal DA release in the terminal regions of nigrostriatal DA neurones. Tolerance develops to this inhibitory e ect during repeated morphine treatment. Furthermore, our results suggest that the e ect of intrastriatally-administered morphine is mediated by the m-opioid receptors.

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Section: Discussionsupporting

confidence: 72%

Characterization of the decrease of extracellular striatal dopamine induced by intrastriatal morphine administration

Piepponen

Mikkola

Ruotsalainen

et al. 1999

British J Pharmacology

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“…Using similar experimental conditions however, Subramanian et al (1977), found that Met-enkephalin in concentrations of 10 -6 and 10 s M significantly diminished the K +-induced (40 mM) release of 3H-dopamine from striatal slices in vitro, an effect which could be blocked by naloxone. The reason for this discrepancy is not known, although it has been suggested that the K+-concentration used by Loh et al (1976) might be aphysiologically high (cf. Arbilla and Langer, 1977).…”

Section: Interaction With Brain Catecholam1nesmentioning

confidence: 84%

Section: Interaction With Brain Catecholaminesmentioning

confidence: 99%

“…In 1976 Loh et al reported that fl-endorphin (fl-LPHol_9~) dose dependently inhibited the K+-stimulated release of 3H-dopamine from superfused striatal slices: the effect was obtained with a K + concentration of 53 mM and was antagonized by naloxone. It was in this same paper that Loh et al (1976) reported that Met-enkephalin failed to affect the K+-induced release of 3H-dopamine from striatal slices (see Section 3.1.). In experiments in which a K + concentration of 20 mM was used, which can be considered to be a more physiological condition, Arbilla and Langer (1978), however, were unable to find any effect of fi-endorphin or morphine on the release of 3H-dopamine from striatal slices.…”

Section: Interaction With Brain Catecholaminesmentioning

confidence: 99%

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Interaction of peptides related to ACTH, MSH and β-LPH with neurotransmitters in the brain

Versteeg

1980

Pharmacology & Therapeutics

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“…Van Loon and Kim 2°, on the other hand, observed increased DOPAC and HVA levels in rat striatum following fl-endorphin administration, compatible with increased striatal dopamine turnover. Loh et al 13 observed a decrease in potassium-induced [SH]-dopamine release by striatal slices incubated with f-endorphin. In contrast, Arbilla and Langer 1 did not find an effect of fl-endorphin on this parameter, whereas [ZH]noradrenaline release by cortical slices was diminished.…”

Section: Introductionmentioning

confidence: 99%

Effects of α-endorphin, β-endorphin and (des-tyr1)-γ-endorphin on α-MPT-induced catecholamine disappearance in discrete regions of the rat brain

1979

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SUMMARYFollowing the intracerebroventricular administration of a-endorphin, fl-endorphin and (des-tyrosinet)-y-endorphin in a dose of 100 ng, the a-MPT-induced catecholamine disappearance was found to be altered in discrete regions of the rat brain. In the regions in which a-endorphin exerted an effect, it without exception caused a decrease in catecholamine disappearance. Thus, in rats treated with aendorphin the disappearance of noradrenaline was decreased in the medial septal nucleus, dorsomedial nucleus, central amygdaloid nucleus, subiculum, the ventral part of the nucleus reticularis medullae oblongatae and the A1 region, and that of dopamine in the caudate nucleus, globus pallidus, medial septal nucleus, nucleus interstitialis striae terminalis, paraventricular nucleus, zona incerta and central amygdaloid nucleus, fl-Endorphin was found to decrease noradrenaline disappearance in the ventral part of the nucleus reticularis medullae oblongatae, dopamine disappearance in the lateral septal nucleus and the disappearance of both amines in the rostral part of the nucleus tractus solitarii. Dopamine disappearance was increased in the medial septal nucleus and the zona incerta following fl-endorphin treatment. Following treatment with (des-tyrosinel)-y-endorphin, noradrenaline disappearance was enhanced in the anterior hypothalamic nucleus, whereas dopamine disappearance was increased in the paraventricular nucleus, the zona incerta and the rostral part of the nucleus tractus solitarii. In addition to this the latter peptide also caused a decreased noradrenaline disappearance in the periventricular thalamus and the A7 region. The results fit well with the suggestion that endorphins act as modulators of catecholamine neurotransmission in particular brain regions. The pattern of effects of the endorphins differ from that previously observed following intracerebroventricular administration of methionine-enkephalin. This is in keeping with the notion that the enkephalin containing network in the brain and that containing fl-LPH represent two 86 independent systems with distinct differences in their projections to various brain regions.

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β-Endorphin in vitro inhibition of striatal dopamine release

Cited by 256 publications

References 15 publications

Characterization of the decrease of extracellular striatal dopamine induced by intrastriatal morphine administration

Characterization of the decrease of extracellular striatal dopamine induced by intrastriatal morphine administration

Interaction of peptides related to ACTH, MSH and β-LPH with neurotransmitters in the brain

Effects of α-endorphin, β-endorphin and (des-tyr1)-γ-endorphin on α-MPT-induced catecholamine disappearance in discrete regions of the rat brain

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