The Effects of Acutely Administered Analgesics on the Turnover of Noradrenaline and Dopamine in Various Regions of the Rat Brain

Sugrue, Michael F.

doi:10.1111/j.1476-5381.1974.tb09696.x

Cited by 62 publications

(12 citation statements)

References 25 publications

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“…It is conceivable that microiontophoretically applied morphine might act on specific neuronal receptors and it would therefore be of interest to know whether the excitation or inhibition of neurones could be mimicked by other opiates and blocked by morphine antagonists. Acute administration of morphine has been shown to release noradrenaline from the brain (Gunne, 1959), increase noradrenaline turnover in the brain stem (Sugrue, 1973) and inhibit its uptake (Ciofalo & Lucero, 1972).…”

Section: Discussionmentioning

confidence: 99%

Morphine and Neurotransmitter Substances: Microiontophoretic Study in the Rat Brain Stem

Bradley¹,

Dray

1974

British J Pharmacology

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The effects of microiontophoretically applied morphine and its interactions with the effects of microiontophoretic applications of either acetylcholine, (–)‐noradrenaline or 5‐hydroxytryptamine have been studied on single neurones in the brain stem of rats anaesthetized with urethane. Morphine excited or inhibited most neurones tested and the effects, especially excitation, were often extremely powerful. However, the time course of the excitatory and inhibitory effects were somewhat different. Desensitization to the excitation produced by morphine was seen after repeated or prolonged applications and it is suggested that this phenomenon may be related to the tolerance which develops after chronic administration of morphine. No desensitization was observed to inhibition of neuronal activity by morphine. Morphine usually reduced the excitation of neurones by acetylcholine, noradrenaline or 5‐hydroxytryptamine but sometimes potentiated the effect, although not always on the same neurones. Inhibition of neuronal activity by these compounds was never modified by morphine and neither were the effects of glutamate or D,L‐homocysteic acid when used as control agonists. The in vitro release of morphine from six micropipettes was determined and the transport number was calculated to be 0.051 (s.d. 0.021). The implications of these observations in explaining the pharmacological actions of morphine are discussed.

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Section: Discussionmentioning

confidence: 99%

Morphine and Neurotransmitter Substances: Microiontophoretic Study in the Rat Brain Stem

Bradley¹,

Dray

1974

British J Pharmacology

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“…However, it is shown that administration of morphine before a-MpT, like in the experiments by Puri et al (1973) and Sugrue (1974), resulted in increased loss of DA in the striatum while administration of morphine a~er pretreatment with e-MpT was without effect (Table 2). Why the effect of morphine in the striatum is different depending on its administration before or a~er e-MpT (Table 2) remains to be clarified.…”

Section: Discussionmentioning

confidence: 75%

“…Since an increased loss of DA induced by morphine has been observed in the rat striatum, when morphine was administered before a-MpT (Puri et al, 1973;Sugrue, 1974), but not when morphine was administered a~er a-MpT (Molernan and Bruinvels, 1976), we first evaluated the effect under both these treatment schedules in the forebrain cortex and compared it with the striatum.…”

Section: Resultsmentioning

confidence: 99%

Effect of morphine on dopaminergic neurons in the rat basal forebrain and striatum

Moleman

Bruitivels

1979

J. Neural Transmission

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Administration of morphine (20 mg/kg i.p.) resulted in an increase in the rate of dopamine (DA) loss by ca. 40% in the forebrain cortex of rats, when the drug was administered 30 min after treatment with the synthesis inhibitor alpha-methyl-para-tyrosine methylester (alpha-MpT). This effect was specific as it was antagonized by naloxone. In the same rats the rate of DA loss in the striatum was unaltered. It was shown that this differential effect was not due to a delayed inhibition of DA synthesis in the forebrain cortex when compared with the striatum. When morphine, on the other hand, was administered before inhibition of DA biosynthesis (30 min before alpha-MpT) an increase in the rate of DA loss was also observed in the striatum and a more marked increase was seen in the forebrain cortex. Sub-dissection of the forebrain cortex showed that most of the DA (80%) was present in basal parts of the forebrain and not in the frontal or cingulate cortex. The results suggest, therefore, that morphine administration results in DA release in basal parts of the forebrain, but not in the striatum.

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“…Morphine exerts effects on several central monoaminergic neuronal systems (Roffman et al, 1970;Yarbrougb et al, 1971;Lob et aL, 1973;Ford et aL, 1974;Korf et aL, 1974;Sugrue, 1974;Simon et aL, 1975;Deyo et aL, 1979;Ivaarnoto and Way, 1979;A&er et aL, 1980). Acute administration of morphine has been shown to increase the turnover and synthesis of 5-hydroxytryptamine (5-HT) in whole brain (Neffet aL, 1967;Yarbrough et aL, 1971;Goodlet and Sugrue, 1974;Pgrez-Cruet et aL, 1975) and in whole hypothalamus (Roffman et aL, 1970;Haubrich and Blake, 1973).…”

Section: Introductionmentioning

confidence: 94%

The effect of morphine on 5-hydroxytryptamine synthesis and metabolism in the striatum, and several discrete hypothalamic regions of the rat brain

Johnston

Moore

1983

J. Neural Transmission

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The effects of morphine on 5-hydroxytryptamine (5-HT) synthesis (accumulation of 5-hydroxytryptophan following inhibition of aromatic L-amino acid decarboxylase) and metabolism (concentration of 5-HT and its primary metabolite, 5-hydroxyindole-3-acetic acid [5-HIAA]) were determined in discrete nuclei of the rat brain using high performance liquid chromatography coupled with electrochemical detection (LCEC). Morphine (10 mg/kg, s.c.) increased 5-HT synthesis in the medial preoptic (MPO), suprachiasmatic (SCN) and arcuate (AN) nuclei as well as the striatum (ST) 1 hour following its administration. 5-HT synthesis in the median eminence (ME) was not affected at any time examined. A lower dose of morphine (5 mg/kg) also stimulated 5-HT synthesis in the AN. Although steady state concentrations of 5-HT were not greatly affected by morphine administration, the concentration of 5-HIAA in the AN, MPO, and ST increased following morphine (10 mg/kg, s.c., 1 hour). The increase in 5-HT synthesis observed in the MPO, SCN, AN, and ST 1 hour following morphine involved the activation of opiate receptors as administration of an opiate receptor antagonist, naloxone, blocked this effect. These results, indicate that morphine causes an increase in 5-HT synthesis and metabolism via an opiate receptor-mediated mechanism in the AN, MPO, SCN, and ST but not in the ME.

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The Effects of Acutely Administered Analgesics on the Turnover of Noradrenaline and Dopamine in Various Regions of the Rat Brain

Cited by 62 publications

References 25 publications

Morphine and Neurotransmitter Substances: Microiontophoretic Study in the Rat Brain Stem

Morphine and Neurotransmitter Substances: Microiontophoretic Study in the Rat Brain Stem

Effect of morphine on dopaminergic neurons in the rat basal forebrain and striatum

The effect of morphine on 5-hydroxytryptamine synthesis and metabolism in the striatum, and several discrete hypothalamic regions of the rat brain

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