Opioid receptors and inhibition of dopamine-sensitive adenylate cyclase in slices of rat brain regions receiving a dense dopaminergic input

Heijna, Menno H.; Bakker, Joost M.; Hogenboom, F.; Mulder, Arie H.; Schoffelmeer, Anton N. M.

doi:10.1016/0014-2999(92)90555-i

Cited by 14 publications

(9 citation statements)

References 23 publications

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“…Moreover, as the morphine effects are linked to the nature of the neurons expressing µ, δ, or κ opioid receptors, we have determined here that µ and κ opioidreceptor mRNAs were colocalized in striatonigral neurons containing D1-receptor and Dyn mRNAs. This is consistent with the fact that activation of opioid receptors during chronic morphine treatment, reduces the postsynaptic D1-receptor-mediated effect of dopamine on adenylate cyclase (Eriksson et al, 1991;Heijna et al, 1992). Another possibility would be that the magnitude of the dopamine increase during the morphine dependence is not sufficient to induce changes in the D1-receptor mRNA level.…”

Section: Dependencesupporting

confidence: 76%

See 1 more Smart Citation

Chronic morphine exposure and spontaneous withdrawal are associated with modifications of dopamine receptor and neuropeptide gene expression in the rat striatum

Georges¹,

Stinus

Bloch³

et al. 1999

Eur J of Neuroscience

125

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The influence of chronic morphine and spontaneous withdrawal on the expression of dopamine receptors and neuropeptide genes in the rat striatum was investigated. Morphine dependence was induced by subcutaneous implantation of two morphine pellets for 6 days. Rats were made abstinent by removal of the pellets 1, 2 or 3 days before they were killed. The mRNA levels coding for D1- and D2-dopamine receptors, dynorphin, preproenkephalin A and substance P were determined by quantitative in situ hybridization. The caudate putamen and the nucleus accumbens showed equivalent modifications in dopamine receptor and neuropeptide gene expression. After 6 days of morphine, a decrease in D2-dopamine receptor and neuropeptide mRNA levels was observed (-30%), but there was no change in D1-dopamine receptor mRNA. In abstinent rats, both D1- and D2-dopamine receptor mRNA levels were decreased 1 day after withdrawal (-30% compared with chronic morphine). In contrast, neuropeptide mRNA levels were unaffected when compared with those observed after 6 days of morphine. During the second and third day of withdrawal, there was a gradual return to the levels seen in the placebo-treated group, for both dopamine receptor and neuropeptide mRNAs. Phenotypical characterization of striatal neurons expressing mu and kappa opioid receptor mRNAs showed that, in striatonigral neurons, both mRNAs were colocalized with D1-receptor and Dyn mRNAs. Our results suggest that during morphine dependence, dopamine and morphine exert opposite effects on striatonigral neurons, and that effects occurring on striatopallidal neurons are under dopaminergic control. We also show that withdrawal is associated with a down regulation of the postsynaptic D1 and D2 receptors.

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Section: Dependencesupporting

confidence: 76%

“…This is consistent with the fact that activation of opioid receptors during chronic morphine treatment, reduces the postsynaptic D1‐receptor‐mediated effect of dopamine on adenylate cyclase (Eriksson et al . 1991;Heijna et al . 1992).…”

Section: Discussionmentioning

confidence: 99%

Chronic morphine exposure and spontaneous withdrawal are associated with modifications of dopamine receptor and neuropeptide gene expression in the rat striatum

Georges¹,

Stinus

Bloch³

et al. 1999

Eur J of Neuroscience

125

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“…KOR activation has been shown to inhibit electrically evoked [ 3 H]dopamine release in the nucleus accumbens (Heijna et al, 1992; Yokoo et al, 1992), which also shows that activation of this receptor reduces striatal dopamine transmission. More recently, Chefer et al (2005) showed that the deletion of KOR is associated with an enhancement of basal dopamine release.…”

Section: Dynorphin and Kappa Receptorsmentioning

confidence: 93%

“…A number of animal studies have shown that the administration of a KOR agonist reduces dopamine levels in the striatum and dopamine neuron activity in the nucleus accumbens and ventral tegmental area (Di Chiara and Imperato, 1988; Heijna et al, 1990, 1992; Donzanti et al, 1992; Spanagel et al, 1992; Maisonneuve et al, 1994; Xi et al, 1998; Thompson et al, 2000; Margolis et al, 2003; Zhang et al, 2004b). In fact, KOR activation reduces basal dopamine levels as well as stimulant-induced dopamine release (cocaine) (Spanagel et al, 1990; Maisonneuve et al, 1994; Carlezon et al, 2006; Gehrke et al, 2008).…”

Section: Dynorphin and Kappa Receptorsmentioning

confidence: 99%

Kappa-Opioid Receptor Signaling in the Striatum as a Potential Modulator of Dopamine Transmission in Cocaine Dependence

Trifilieff¹,

Martínez²

2013

Front. Psychiatry

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Cocaine addiction is accompanied by a decrease in striatal dopamine signaling, measured as a decrease in dopamine D2 receptor binding as well as blunted dopamine release in the striatum. These alterations in dopamine transmission have clinical relevance, and have been shown to correlate with cocaine-seeking behavior and response to treatment for cocaine dependence. However, the mechanisms contributing to the hypodopaminergic state in cocaine addiction remain unknown. Here we review the positron emission tomography (PET) imaging studies showing alterations in D2 receptor binding potential and dopamine transmission in cocaine abusers and their significance in cocaine-seeking behavior. Based on animal and human studies, we propose that the kappa receptor/dynorphin system, because of its impact on dopamine transmission and upregulation following cocaine exposure, could contribute to the hypodopaminergic state reported in cocaine addiction, and could thus be a relevant target for treatment development.

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“…In fact, research from our laboratory has previously shown that the benzomorphan drug bremazocine is a potent agonist at a subtype of δ-opioid receptors interacting with µ-opioid receptors (Schoffelmeer et al 1987(Schoffelmeer et al , 1988Heijna et al 1989). These interacting opioid receptors inhibit dopamine D1 receptor-stimulated adenylate cyclase (Schoffelmeer et al 1987(Schoffelmeer et al , 1988(Schoffelmeer et al , 1993Heijna et al 1989Heijna et al , 1992. Thus, by stimulating this δ-receptor subtype, bremazocine may act as a functional dopamine D1 receptor antagonist.…”

Section: Introductionmentioning

confidence: 95%

Dissociable effects of the κ-opioid receptor agonists bremazocine, U69593, and U50488H on locomotor activity and long-term behavioral sensitization induced by amphetamine and cocaine

et al. 2000

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In agreement with previous studies, the present data suggest that differential mechanisms underlie the acute stimulant versus the long-term sensitizing effects of psychostimulants, and the induction of long-term sensitization by amphetamine versus cocaine. Stimulation of kappa-opioid receptors does not seem to block the induction of long-term psychostimulant sensitization. Thus, bremazocine is likely to block the induction of amphetamine sensitization through a non-kappa-opioid receptor mechanism. We suggest that this effect of bremazocine is the result of its unique agonist action at a subtype of delta-opioid receptors, thereby acting as a functional dopamine D1 receptor antagonist. This would be consistent with the literature showing that the induction of long-term amphetamine sensitization depends on the activation of dopamine D1 receptors. In addition, the present data are in keeping with studies showing that dopamine neurotransmission is not critical for the induction of long-term cocaine sensitization.

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Opioid receptors and inhibition of dopamine-sensitive adenylate cyclase in slices of rat brain regions receiving a dense dopaminergic input

Cited by 14 publications

References 23 publications

Chronic morphine exposure and spontaneous withdrawal are associated with modifications of dopamine receptor and neuropeptide gene expression in the rat striatum

Chronic morphine exposure and spontaneous withdrawal are associated with modifications of dopamine receptor and neuropeptide gene expression in the rat striatum

Kappa-Opioid Receptor Signaling in the Striatum as a Potential Modulator of Dopamine Transmission in Cocaine Dependence

Dissociable effects of the κ-opioid receptor agonists bremazocine, U69593, and U50488H on locomotor activity and long-term behavioral sensitization induced by amphetamine and cocaine

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