Repeated stimulation of dopamine D1 receptors enhances the effects of dopamine receptor agonists

White, Francis J.; Hu, Xiu‐Ti; Brooderson, Richard J.

doi:10.1016/0014-2999(90)94188-4

Cited by 31 publications

(11 citation statements)

References 5 publications

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“…Together these results suggest that repeated stimulation of the dopamine Dl-type receptor alone is sufficient to induce the development of behavioral sensitization to the mixed dopamine agonist apomorphine. Based upon both behavioral and electrophysiological data, other researchers have also concluded that repeated dopamine D1 receptor stimulation may be the crucial factor neccessary for the induction of agonist-induced behavioral sensitization (e.g., Braun and Chase 1988;Criswell et al 1989;Henry et al 1989;Stewart and Vezina 1989;Vezina and Stewart 1989;White et al 1990;Henry and White 1991). It should be noted, however, that SKF 38393 is not a full but rather a partial D~ dopamine receptor agonist.…”

Section: Discussionmentioning

confidence: 95%

“…As noted previously, the SKF 38393-induced decrease in locomotor activity did not significantly change with repeated treatments. Likewise, SKF 38393-induced grooming behavior in rats does not significantly increase with daily treatments (White et al 1990;Niesewander et al 1991). Thus, the possibility exists that the hypoactivity observed after mixed agonist treatments is mediated in part by D1 receptors (cf, Vezina et al 1991).…”

Section: Discussionmentioning

confidence: 96%

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Effects of daily SKF 38393, quinpirole, and SCH 23390 treatments on locomotor activity and subsequent sensitivity to apomorphine

1993

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In three experiments, male Wistar rats (250-350 g) were injected (SC) daily with the D1-type dopamine receptor agonist, SKF 38393 (0.0, 4.0, 8.0, or 16.0 mg/kg), the D2-type dopamine receptor agonist, quinpirole (0.0, 0.3, or 3.0 mg/kg), and/or the D1-type dopamine receptor antagonist, SCH 23390 (0.0 or 0.5 mg/kg) for 8-10 days. After each daily injection, the rats were tested for locomotor activity in photocell arenas for 20 min. Following this subchronic pretreatment, all rats were challenged with the mixed dopamine receptor agonist apomorphine (1.0 mg/kg, SC) and tested for locomotor activity. SKF 38393 treatments produced a dose-dependent decrease in locomotor activity which did not significantly change across days. Quinpirole also depressed locomotor activity when first injected, but this quinpirole-induced inhibition of activity progressively decreased across days. When subsequently challenged with apomorphine, rats in both the SKF 38393 and the quinpirole pretreatment groups displayed greater locomotor activity than rats pretreated with only vehicle. Although SCH 23390 pretreatments did not affect subsequent sensitivity to apomorphine, SCH 23390 completely blocked the effect of quinpirole. These results suggest that although repeated D1 receptor stimulation may be sufficient to induce behavioral sensitization to apomorphine, D2 receptor stimulation also contributes to the effect.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 96%

Effects of daily SKF 38393, quinpirole, and SCH 23390 treatments on locomotor activity and subsequent sensitivity to apomorphine

1993

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“…If DA autoreceptor subsensitivity is prevented, more slowly developing adaptations in the NAc, linked to expression of behavioral sensitization and its persistence, do not occur (Wolf et al, 1994; Li et al, 1999). Furthermore, repeated treatment with a D1 receptor agonist, which does not produce DA autoreceptor sensitivity, fails to produce lasting sensitization (White et al, 1990; Hu et al, 1992). Third, cocaine, amphetamine, and stress, which produce cross-sensitization, all produce transient DA autoreceptor subsensitivity in the VTA (White, 1996; Marinelli, 2007).…”

Section: Cp-ampars In the Vtamentioning

confidence: 99%

Calcium-permeable AMPA receptors in the VTA and nucleus accumbens after cocaine exposure: when, how, and why?

Wolf¹,

Tseng²

2012

Front. Mol. Neurosci.

187

219

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In animal models of drug addiction, cocaine exposure has been shown to increase levels of calcium-permeable AMPA receptors (CP-AMPARs) in two brain regions that are critical for motivation and reward—the ventral tegmental area (VTA) and the nucleus accumbens (NAc). This review compares CP-AMPAR plasticity in the two brain regions and addresses its functional significance. In VTA dopamine neurons, cocaine exposure results in synaptic insertion of high conductance CP-AMPARs in exchange for lower conductance calcium-impermeable AMPARs (CI-AMPARs). This plasticity is rapid in onset (hours), GluA2-dependent, and can be observed with a single cocaine injection. Whereas it is short-lived after experimenter-administered cocaine, it persists for months after cocaine self-administration. In addition to strengthening synapses and altering Ca2+ signaling, CP-AMPAR insertion alters subsequent induction of plasticity at VTA synapses. However, CP-AMPAR insertion is unlikely to mediate the increased DA cell activity that occurs during early withdrawal from cocaine exposure. Metabotropic glutamate receptor 1 (mGluR1) exerts a negative influence on CP-AMPAR accumulation in the VTA. Acutely, mGluR1 stimulation elicits a form of LTD resulting from CP-AMPAR removal and CI-AMPAR insertion. In medium spiny neurons (MSNs) of the NAc, extended access cocaine self-administration is required to increase CP-AMPAR levels. This is first detected after approximately a month of withdrawal and then persists. Once present in NAc synapses, CP-AMPARs mediate the expression of incubation of cue-induced cocaine craving. The mechanism of their accumulation may be GluA1-dependent, which differs from that observed in the VTA. However, similar to VTA, mGluR1 stimulation removes CP-AMPARs from MSN synapses. Loss of mGluR1 tone during cocaine withdrawal may contribute to CP-AMPAR accumulation in the NAc. Thus, results in both brain regions point to the possibility of using positive modulators of mGluR1 as treatments for cocaine addiction.

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“…There is evidence that pre-as well as postsynaptic alterations in dopaminergic neurotransmission are relevant for the manifestation of the sensitization phenomena. After repeated administration of an agonist either at dopamine D 1 -like receptors (White et al 1990) or, at least under certain experimental conditions, a D 2 agonist (Martin-Iverson et al 1988), the behavioural response to an agonist at dopamine receptors is enhanced.…”

Section: Introductionmentioning

confidence: 99%

Sensitization phenomena after repeated administration of cocaine or D-amphetamine in rats: associative and non-associative mechnisms and the role of dopamine in the striatum

Lienau

Kuschinsky

1997

Naunyn-Schmiedeberg's Arch Pharmacol

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In parallel studies, the contribution of non-associative and associative mechanisms to the development of sensitization to the effects of cocaine and D-amphetamine on locomotor activity and stereotyped behaviour were tested. Rats were pretreated with cocaine, 10 mg/kg s.c. twice, D-amphetamine 1.5 mg/kg s.c. once or with saline. During the pretreatment period, one group of rats was administered the drug in positive temporal association with conditional stimuli (CS) ('associative'), another group in negative temporal association with the CS ('non-associative'), a saline pretreated control group was exposed to the CS but administered the drug only during the test ('naive'). On the test day, 7 days after the last drug administration, in the cocaine-sensitized group, cocaine produced the largest locomotor stimulation and the highest scores of stereotypies (mainly sniffing) in the 'associative' group, significantly smaller effects in the 'non-associative' group, and the smallest effects in the 'naive' group. The stereoypies (mainly licking) produced by D-amphetamine in the amphetamine-sensitized group on the test day, 7 days after the last drug administration, were also most pronounced in the 'associative' group, less pronounced in the 'non-associative' group and least in the 'naive' group, whereas the opposite sequences of intensities were found with regard to locomotor activation. The observations in D-amphetamine-treated groups suggest that there is a negative correlation between locomotor activity and stereotyped licking. Estimation of the extracellular dopamine using microdialysis in the striatum showed no significant differences between the three cocaine groups in the moderate increases. In contrast, after D-amphetamine treatment, the strong increases in dopamine were most pronounced in the 'associative' group, significantly less in the 'non-associative' group and even less in the 'naive' group. The biochemical findings in the D-amphetamine-pretreated animals are apparently related to the pronounced stereotyped licking observed in these animals which is probably induced in the striatum, whereas locomotor activation and sniffing are probably mediated elsewhere and therefore are not reflected biochemically in the striatum.

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Repeated stimulation of dopamine D1 receptors enhances the effects of dopamine receptor agonists

Cited by 31 publications

References 5 publications

Effects of daily SKF 38393, quinpirole, and SCH 23390 treatments on locomotor activity and subsequent sensitivity to apomorphine

Effects of daily SKF 38393, quinpirole, and SCH 23390 treatments on locomotor activity and subsequent sensitivity to apomorphine

Calcium-permeable AMPA receptors in the VTA and nucleus accumbens after cocaine exposure: when, how, and why?

Sensitization phenomena after repeated administration of cocaine or D-amphetamine in rats: associative and non-associative mechnisms and the role of dopamine in the striatum

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