Opioid regulation of CNS dopaminergic pathways: A review of methodology, receptor types, regional variations and species differences

Wood, Paul L.

doi:10.1016/0196-9781(83)90003-7

Cited by 128 publications

(32 citation statements)

References 38 publications

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“…This result provides pharmacogenetic evidence for cross-talk between the opioid and dopamine systems, as has been suggested by other studies. 20,[27][28][29]41,42 On the other hand, the SNP A118G was not significantly associated with MAP dependence/psychosis, as shown in our previous report. 30 These results, taken together with the fact that the SNP A118G was found only in the coding regions of the OPRM1 gene in Japanese subjects, could suggest that polymorphisms in the non-coding regions rather than in the coding regions of the OPRM1 gene affect MAP dependence/ psychosis.…”

Section: Discussionmentioning

confidence: 63%

“…19 The increase in dopamine release through dopamine transporters owing to MAP is primarily responsible for the induction of its reinforcing and psychogenic effects. Opioid receptor agonists are known to affect dopamine neurotransmission 20 and to attenuate MAP-induced enhance-ment of dopamine neurotransmission. 21,22 Naloxone, an opioid receptor antagonist, potentiated the long-lasting dopamine depletion produced by MAP.…”

Section: Introductionmentioning

confidence: 99%

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Linkage disequilibrium and association with methamphetamine dependence/psychosis of μ-opioid receptor gene polymorphisms

et al. 2006

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Several studies indicate that the m-opioid receptor plays a role in addiction not only to opiate drugs but also to alcohol and non-opiate addictive drugs. Our studies aim to reveal the associations between gene polymorphisms and methamphetamine (MAP) dependence/psychosis. We newly identified several polymorphisms and four substantial linkage disequilibrium (LD) blocks in the m-opioid receptor (OPRM1) gene. We found significant differences in both genotype and allele frequencies of the single-nucleotide polymorphism (SNP) IVS2 þ G691C between control (n ¼ 232) and MAPdependent/psychotic patients (n ¼ 128). There was also a significant association between IVS2 þ G691C and patients with transient psychosis. These results suggest that the OPRM1 gene variations may be a factor in development and prognosis of MAP psychosis.

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Section: Discussionmentioning

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Linkage disequilibrium and association with methamphetamine dependence/psychosis of μ-opioid receptor gene polymorphisms

et al. 2006

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“…Although the mechanism of this neurochemical potentiation is not currently known, several lines of evidence suggest interactions between opiates and stimulants (Stinus et al, 1992;Wood, 1983). Opioid receptors are located on a subset of dopaminergic neurons within the mesolimbicmesocortical systems (Goodman et al, 1988;Mansour et al, 1988;Sharif and Hughes, 1989;Garzón and Pickel, 2001), while the majority of m-opioid receptors in the VTA are located on GABAergic interneurons (Garzon and Pickel, 2001).…”

Section: Potential Mechanismsmentioning

confidence: 99%

Self-Administered Heroin and Cocaine Combinations in the Rat: Additive Reinforcing Effects—Supra-Additive Effects on Nucleus Accumbens Extracellular Dopamine

Smith

Coller

et al. 2005

Neuropsychopharmacol

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The concurrent use of cocaine and opiate combinations (speedball) has increased since the 1970s and now represents a growing subset of intravenous drug abusers. An isobolographic analysis was applied to the ascending limb of the dose-effect curves for rat selfadministration of cocaine, heroin, and their combination to determine the nature of the interaction. The addition of heroin to cocaine shifted the dose-effect curve for self-administration to the left, and the modulation in reinforcing efficacy of the combination of cocaine and heroin was found to be additive. A second experiment used microdialysis to determine the effects of this drug combination on nucleus accumbens (NAc) extracellular levels of dopamine ([DA] e ) in rats self-administering low doses of cocaine, heroin, or cocaine/ heroin combinations. These doses of cocaine and cocaine/heroin combinations significantly increased NAc [DA] e , while heroin alone did not. The ratio of the % baseline of [DA] e (or the dialysate concentrations of DA) to cocaine in the dialysate was higher during selfadministration of cocaine/heroin combinations than with cocaine alone. These data indicate that although the interaction between cocaine and heroin in maintaining self-administration is additive, a potentiation of NAc dopaminergic neurotransmission is present, suggesting that NAc [DA] e may not be a direct measure of reinforcing efficacy and/or it is not central to the mediation of the selfadministration of this drug combination.

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“…The neostriatum, the major target region for information transmitted by dopaminergic neurons arising from the substantia nigra (Dray, 1979), contains a large number of enkephalinergic neurons (Cuello, 1983;Hughes et al, 1977;Yang et al, 1977), as well as a high density of opioid receptors, particularly those of the 6-and p-types (Atweh and Kuhar, 1983;Wamsley, 1983). A variety of circumstantial evidence suggests that modulation of dopaminergic neurotransmission plays a role in the action of opioids on the CNS (Chesselet et al, 198 1;Hirschhom et al, 1983;Iwamato and Way, 1979;Mulderet al, 1984;Wood, 1983) and may, in fact, also be one of the functional consequences of release of endogenous opioid peptides.…”

mentioning

confidence: 99%

“…The neostriatum, the major target region for information transmitted by dopaminergic neurons arising from the substantia nigra (Dray, 1979), contains a large number of enkephalinergic neurons (Cuello, 1983;Hughes et al, 1977;Yang et al, 1977), as well as a high density of opioid receptors, particularly those of the 6-and p-types (Atweh and Kuhar, 1983; Wamsley, Received Sept. 30, 1985; revised Jan. 23, 1986; accepted Jan. 24, 1986. Correspondence should be addressed to Anton N. Iwamato and Way, 1979; Mulderet al, 1984;Wood, 1983) and may, in fact, also be one of the functional consequences of release of endogenous opioid peptides. In the neostriatum, 2 pharmacologically and functionally different types ofdopamine receptors have been demonstrated, i.e., D-1 and D-2 (Creese et al, 1983;Kebabian and Calne, 1979;Seeman, 1980; Stoof and Kebabian, 198 1).…”

mentioning

confidence: 99%

Blockade of D-2 dopamine receptors strongly enhances the potency of enkephalins to inhibit dopamine-sensitive adenylate cyclase in rat neostriatum: involvement of delta- and mu-opioid receptors

Schoffelmeer¹,

Hansen²,

Stoof³

et al. 1986

J. Neurosci.

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The interactions between dopamine receptors and opioid recep tors coupled to adenylate cyclase in rat neostriatum were investigated. CAMP efflux from neostriatal slices induced by simultaneous activation of (stimulatory) D-l and (inhibitory) D-2 dopamine receptors with 30 PM dopamine was inhibited by the preferential &opioid receptor agonist [r+Ala*-D-LeuS] enkephalin (DADLE) and the cc-opioid receptor agonist morphine with an EC, of 100 and 800 nM, respectively. On selective D-l receptor activation (i.e., with D-2 receptors blocked by 10 e(~ (-)sulpiride), the EC, of DADLE was strongly reduced to 3 nM, whereas that of morphine was unaffected. When D-l and D-2 receptors were activated simultaneously, the inhibitory effects of DADLE (0.3 PC(M) and morphine (3 PM) on CAMP efflux were antagonized equally well by naloxone, a p-opioid receptor antagonist. In contrast, on selective D-l receptor activation, naloxone was about 20 times more potent in antagonizing the inhibitory effect of morphine than DADLE. Moreover, the &opioid receptor antagonist ICI 174864 (0.75 PM) did not affect the inhibitory effect of morphine but antagonized that of DADLE, provided that D-2 receptors were blocked. The highly selective b-opioid receptor agonist [D-Pen*+-Pens] enkephalin (DPDPE) inhibited dopamine-stimulated CAMP efflux only when D-2 receptors were blocked. Similar results were obtained when the agonists SKF 38393 and LY 141865 were used to activate D-l and D-2 receptors, respectively.These data indicate that blockade of D-2 receptors in the neostriatum elicits the coupling of bopioid receptors to dopamine-sensitive adenylate cyclase, thereby making it considerably more sensitive to inhibition by the enkephalins.Opioid receptors in peripheral tissues and in the CNS can be distinguished pharmacologically in at least 3 different typesviz., p(morphine), G(enkephalin), and K(benzomorphan/dynorphin) receptors-but the functional implications of this receptor multiplicity are still largely unknown (Chang et al., 198 1;Gillan and Kosterlitz, 1982;Lord et al., 1977;Martin, 1984; Mulder et al., 1984;Paterson et al., 1983;Wood, 1982; Wiister et al., 198 1). The neostriatum, the major target region for information transmitted by dopaminergic neurons arising from the substantia nigra (Dray, 1979), contains a large number of enkephalinergic neurons (Cuello, 1983;Hughes et al., 1977;Yang et al., 1977), as well as a high density of opioid receptors, particularly those of the 6-and p-types (Atweh and Kuhar, 1983; Wamsley, Received Sept. 30, 1985; revised Jan. 23, 1986; accepted Jan. 24, 1986. Correspondence should be addressed to Anton N. Iwamato and Way, 1979; Mulderet al., 1984;Wood, 1983) and may, in fact, also be one of the functional consequences of release of endogenous opioid peptides. In the neostriatum, 2 pharmacologically and functionally different types ofdopamine receptors have been demonstrated, i.e., D-1 and D-2 (Creese et al., 1983;Kebabian and Calne, 1979;Seeman, 1980; Stoof and Kebabian, 198 1). Activation of D-l receptor...

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Opioid regulation of CNS dopaminergic pathways: A review of methodology, receptor types, regional variations and species differences

Cited by 128 publications

References 38 publications

Linkage disequilibrium and association with methamphetamine dependence/psychosis of μ-opioid receptor gene polymorphisms

Linkage disequilibrium and association with methamphetamine dependence/psychosis of μ-opioid receptor gene polymorphisms

Self-Administered Heroin and Cocaine Combinations in the Rat: Additive Reinforcing Effects—Supra-Additive Effects on Nucleus Accumbens Extracellular Dopamine

Blockade of D-2 dopamine receptors strongly enhances the potency of enkephalins to inhibit dopamine-sensitive adenylate cyclase in rat neostriatum: involvement of delta- and mu-opioid receptors

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