Differential enhancement of locomotor activity by dopamine agonists following chronic morphine treatment

Tye, N. C.; Horsman, Linda; Wright, Francesca; Pullar, Ian A.

doi:10.1007/bf00433570

Cited by 4 publications

(1 citation statement)

References 2 publications

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“…Trujillo and Akil (1990) reported significant increases in , 1988). An increase in the supersensitivity of D, receptors and D, stimulated CAMP production has been shown in striatum (Ritzmann et al, 1982;Tye et al, 1979;Merali et al, 1976;DeVries et al, 1991). Chronic morphine may activate the hypothalamus-pituitary-adrenal axis and also the mesolimbic dopaminergic system with an increased numberisensitivity of Gas-associated receptors which in return warrant increased levels of G,, protein.…”

Section: Gsmentioning

confidence: 97%

Morphine‐induced reciprocal alterations in G_αs and opioid peptide mRNA levels in discrete brain regions

Basheer

Tempel

1993

J of Neuroscience Research

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The mechanisms involved in the development of morphine tolerance and dependence are still unknown. Recently much attention has been directed toward the changes in post receptor events. Opiate receptors, like other hormone and neurotransmitter receptors, have been shown to mediate their effects through guanine nucleotide binding proteins (G-proteins). This, in turn, may cause alterations in intracellular events, one of which is transcription of specific genes. We investigated the changes in the levels of mRNA of proenkephalin (PPE) and prodynorphin (DYN) and the stimulatory G protein alpha subunit (G alpha s) in adult morphine tolerant rats. Chronic morphine treatment induced reciprocal alterations in the levels of opioid peptide mRNA and G alpha s mRNA in discrete brain regions. In striatum, PPE mRNA decreased by 49% (P < .01) and in hypothalamus, DYN mRNA showed a decrease of 21% (P < .01). In contrast, G alpha s mRNA increased 20% (P < .01) in striatum and 97% (P < .01), in hypothalamus. In hippocampus the changes were reversed: PPE mRNA increased (55%, P < .05) and G alpha s mRNA decreased (33%, P < .01). Frontal cortex exhibited a small decrease in PPE (11.5%, P < .05) without any change on G alpha s or DYN mRNA levels. These reciprocal alterations suggest an opposing mode of regulation of G alpha s and PPE/DYN gene expression in morphine tolerant animals.

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Section: Gsmentioning

confidence: 97%

Morphine‐induced reciprocal alterations in G_αs and opioid peptide mRNA levels in discrete brain regions

Basheer

Tempel

1993

J of Neuroscience Research

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Role of dopamine receptors in the dual effect of naloxone on quinpirole-induced yawning in morphine pretreated rats

Zharkovsky

Moisio

Kivastik

et al. 1993

Naunyn-Schmiedeberg's Arch Pharmacol

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The present study was undertaken to determine the state of sensitivity of dopamine D2/D3 receptors involved in the mediation of yawning behaviour at various times following acute morphine administration to rats. Morphine (3.0 mg/kg, s.c.) induced a biphasic effect on locomotor activity: an initial inhibitory phase lasting for about 30 min was after about an hour followed by a phase of locomotor activation lasting for about 60 min. Dopamine D2/D3 receptor agonist quinpirole (0.01-0.1 mg/kg, s.c.) induced yawning behaviour in rats. Morphine given at 15 or 60 min before (inhibitory phase) inhibited the yawning response to quinpirole (0.1 mg/kg) but not when given at 90 or 120 min before (stimulatory phase). Naloxone (1.0 mg/kg) given 10 min before quinpirole restored yawning inhibited by morphine pretreatment during the inhibitory phase (15-60 min after morphine). However, during the morphine-induced stimulatory phase naloxone strongly inhibited the yawning response to quinpirole. D1 receptor antagonist SCH 23390 [R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3- benzazepin-7-ol hemimaleate] at 0.01 mg/kg did not affect quinpirole-induced yawning or its inhibition by morphine. However, in rats which received morphine 90 min prior to testing yawning, SCH 23390 enhanced quinpirole-induced yawning behaviour as compared with morphine- or saline-pretreated animals. The data obtained in the present study indicate that morphine pretreatment initially induces a lack of responsiveness of the D2/D3 receptors mediating yawning behaviour and subsequently increases their sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

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Differential enhancement of locomotor activity by dopamine agonists following chronic neuroleptic treatment: an animal model of tardive dyskinesia

Tye¹,

Horsman²,

Wright³

et al. 1979

European Journal of Pharmacology

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Differential enhancement of locomotor activity by dopamine agonists following chronic morphine treatment

Cited by 4 publications

References 2 publications

Morphine‐induced reciprocal alterations in G_αs and opioid peptide mRNA levels in discrete brain regions

Morphine‐induced reciprocal alterations in G_αs and opioid peptide mRNA levels in discrete brain regions

Role of dopamine receptors in the dual effect of naloxone on quinpirole-induced yawning in morphine pretreated rats

Differential enhancement of locomotor activity by dopamine agonists following chronic neuroleptic treatment: an animal model of tardive dyskinesia

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Differential enhancement of locomotor activity by dopamine agonists following chronic morphine treatment

Cited by 4 publications

References 2 publications

Morphine‐induced reciprocal alterations in Gαs and opioid peptide mRNA levels in discrete brain regions

Morphine‐induced reciprocal alterations in Gαs and opioid peptide mRNA levels in discrete brain regions

Role of dopamine receptors in the dual effect of naloxone on quinpirole-induced yawning in morphine pretreated rats

Differential enhancement of locomotor activity by dopamine agonists following chronic neuroleptic treatment: an animal model of tardive dyskinesia

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Morphine‐induced reciprocal alterations in G_αs and opioid peptide mRNA levels in discrete brain regions

Morphine‐induced reciprocal alterations in G_αs and opioid peptide mRNA levels in discrete brain regions