Modulation of acetylcholine release by D1, D2 dopamine receptors in rat striatum under freely moving conditions

doi:10.1016/0006-8993(90)90972-E

Brain Research

Volume 518, Issues 1–2, 4 June 1990, Pages 193-198

https://doi.org/10.1016/0006-8993(90)90972-E Get rights and content

Abstract

Using in vivo brain dialysis under freely moving conditions, we have studied the effects of dopamine (DA) agonists and antagonists on acetylcholine (ACh) and DA release in rat striatum. The striatal infusion of the D₁ DA receptor specific agonist, SKF38393, increased striatal ACh release in a dose-dependent manner (10⁻⁶ to 10⁻⁴ M), and 3 × 10⁻⁵ M SKF38393 elicited a 60% augmentation in the level of ACh release. The level of ACh was increased with perfusion of 10⁻⁴ M SCH23390, a D₁ specific antagonist, but decreased with 10⁻³ M SCH23390. The D₂ specific agonist, LY171555, and the antagonist, sulpiride, slightly altered the level of ACh in the striatum. On the other hand the level of DA dramatically increased in a dose-dependent manner with SKF38393 or SCH23390 and decreased with LY171555. LY171555 inhibited the effect of 10⁻⁴ M SKF38393 on ACh release, and enhanced the effect of SKF38393 on DA release. These results suggest that the D₁ DA receptor mainly mediates ACh release and the D₂ DA receptor modifies the effects of the D₁ receptor.

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Dopamine D<inf>1</inf>-like receptors play only a minor role in the increase of striatal dopamine induced by striatally applied SKF38393
2010, European Journal of Pharmacology
Citation Excerpt :
SKF38393, a benzazepine derivative dopamine D1-like receptor agonist, is known to produce a transient increase of the striatal extracellular concentration of dopamine when locally applied into the rat striatum (Ajima et al., 1990; Kurata and Shibata, 1991; Saigusa et al., 2009; Tomiyama et al., 1995).
We studied the effects of the intra-striatal infusion of Ca²⁺-free medium on the intra-striatal injection of 0.5 μg SKF38393-induced striatal dopamine efflux. It is discussed that the amount of extracellular, striatal dopamine seen after striatally applied SKF38393, is the overall result of the (a) release of dopamine from the alpha-methyl-para-tyrosine-sensitive and Ca²⁺-insensitive pool of newly synthesised dopamine, (b) release of dopamine from the reserpine-sensitive and Ca²⁺-sensitive storage pool, (c) inhibition of uptake of dopamine into nerve terminals and glial cells, and (d) facilitation respectively of the inhibition of uptake into blood vessels: dopamine D₁-like receptors play only a very limited role in these processes. The present study underlines our previous notion that the effects of SKF38393 cannot simply be ascribed to the dopamine D₁-like receptor stimulation (Saigusa et al., 2009): in fact, the present study clearly reveals that SKF38393 is not at all selective in that respect.
Contribution of vesicular and cytosolic dopamine to the increased striatal dopamine efflux elicited by intrastriatal injection of SKF38393
2009, European Journal of Pharmacology
Citation Excerpt :
SKF38393, a benzazepine derivative dopamine D1 receptor agonist, is known to produce a transient increase of the striatal extracellular concentration of dopamine when locally applied into the rat striatum (Ajima et al., 1990; Kurata and Shibata, 1991; Tomiyama et al., 1995).
Like dexamphetamine, SKF38393 induces an increase in striatal dopamine efflux which is insensitive for tetrodotoxin, Ca²⁺ independent and prevented by a dopamine transporter inhibitor. The dexamphetamine-induced striatal dopamine efflux originates from both the reserpine-sensitive vesicular dopamine pool and the alpha-methyl-para-tyrosine-sensitive cytosolic dopamine pool. Given the similarities between dexamphetamine and SKF38393, we hypothesized that both types of pool also contribute to the striatally applied SKF38393-induced dopamine efflux. Using in vivo microdialysis technique, we analysed the contribution of these pools to the SKF38393-induced striatal dopamine efflux in freely moving rats. The increase of dopamine efflux induced by 1.5 μg SKF38393 was largely prevented by either reserpine (5 mg/kg i.p., given 24 h earlier) or alpha-methyl-para-tyrosine (250 mg/kg i.p., given 2 h earlier), showing that both the vesicular dopamine pool and the cytosolic dopamine pool contribute to the SKF38393-induced increase in striatal dopamine efflux. The sum of the amounts of dopamine that was sensitive to either reserpine or alpha-methyl-para-tyrosine, was greater than 100%, namely 137.6% of the basal dopamine level and 143.9% of the SKF38393-induced dopamine level, suggesting that striatally applied SKF38393 promotes the redistribution of dopamine from vesicles to the cytosol, and vice versa. The finding that the combined treatment of reserpine and alpha-methyl-para-tyrosine only inhibited the SKF38393-induced striatal dopamine efflux till 86.0% of the control, is ascribed to the notion that SKF38393 can also inhibit the re-uptake of dopamine. The latter conclusion has far-reaching consequences for studies in which the effects of SKF38393 are simply ascribed to its dopamine D₁ receptor stimulation capacity.
Muscarinic, adenosine A<inf>2</inf> and histamine H<inf>3</inf> receptor modulation of haloperidol-induced c-fos expression in the striatum and nucleus accumbens
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It is generally believed that haloperidol exerts its motor side effects and therapeutic effects mainly by antagonizing dopamine D₂ receptors in the striatum and the nucleus accumbens, respectively. Several neurotransmitters/modulators, including glutamate, acetylcholine, adenosine and histamine, affect dopaminergic activity in these centers. We have recently shown that N-methyl-D-aspartate receptor-mediated modulation of haloperidol-induced c-fos expression differs in functionally specific regions of the striatum and the nucleus accumbens. In the present study, the entire striatum and the nucleus accumbens were comprehensively examined for the pattern of modulation of haloperidol-induced c-fos expression by adenosine A₂, histamine H₃ and muscarinic receptor antagonists.
Blockade of muscarinic and H₃ receptors resulted in a profound suppression of haloperidol-induced c-fos expression in the dorsolateral part of the striatum. In addition, the H₃ receptor antagonist suppressed the effects of haloperidol in the ventrolateral aspect of the striatum and the rostral parts of the medial striatum. Muscarinic receptor antagonists suppressed haloperidol-induced c-fos expression throughout the shell and in the mid-level of the core of the nucleus accumbens while A₂ and H₃ receptor antagonists did not.
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Caudate-putamen and nucleus accumbens extracellular acetylcholine responses to methamphetamine binges
2001, Brain Research
Citation Excerpt :
With regard to the influence of specific dopaminergic mechanisms on ACh responsivity, it appears that D1 and D2 dopamine receptor subtypes exert an opposing modulation of caudate-putamen ACh function [14,17,19,37,50]. Although the location of the population of D1 receptors regulating caudate-putamen ACh release has not been identified [2,4–6,15,18], the ACh response to METH likely reflects, at least in part, the relative activation of D1 and D2 dopamine receptors. Therefore, the changes in ACh concentration and the corresponding decrease in stereotypy that result from multiple binge exposures could be due to a decrease in D2 and/or an increase in D1 receptor activation.
Exposure of experimental animals to an escalating dose, multiple binge pattern of methamphetamine administration results in the progressive emergence of a unique behavioral profile, which includes a significant decrease in the duration of the stereotypy phase as well as a profound increase and qualitative change in the locomotor activation. This behavioral profile is associated with a selective decrease in the caudate-putamen but not nucleus accumbens extracellular dopamine response. Since the acetylcholine interneurons in these regions are partly under the control of the mesostriatal and mesoaccumbens dopamine inputs, changes in the activation of these interneurons should parallel the regionally differential dopamine responses during multiple binge treatment. Therefore, we characterized the caudate-putamen and nucleus accumbens extracellular acetylcholine responses to escalating-dose, multiple binge methamphetamine administration. An acute methamphetamine binge decreased acetylcholine levels in caudate-putamen, but had no effect on levels in nucleus accumbens. Furthermore, corresponding to the selective decrease in the dopamine response, the caudate-putamen but not nucleus accumbens extracellular acetylcholine response exhibited tolerance with repeated binge exposures; i.e. the decrease in acetylcholine associated with the acute methamphetamine binge was attenuated with multiple binge exposure. These results are consistent with our hypothesis and suggest that the regionally differential acetylcholine responses reflect one functional consequence of the escalating-dose, multiple binge stimulant treatment.
β-Phenylethylamine modulates acetylcholine release in the rat striatum: Involvement of a dopamine D<inf>2</inf> receptor mechanism
2001, European Journal of Pharmacology
We examined the effects of β-phenylethylamine on striatal acetylcholine release in freely moving rats using in vivo microdialysis. β-Phenylethylamine at 12.5 mg/kg, i.p. did not affect acetylcholine release in the striatum, whereas 25 and 50 mg/kg, i.p. immediately induced an increase in acetylcholine release in the striatum at 15–45 min. This increase following intraperitoneal administration of β-phenylethylamine (25 mg/kg) was not affected by locally applied SCH-23390 (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine, 10 μM), a dopamine D₁ receptor antagonist, nor by raclopride (10 μM), a dopamine D₂ receptor antagonist. The increased release of acetylcholine induced by β-phenylethylamine was suppressed by local infusion of tetrodotoxin (1 μM). In contrast, the extracellular acetylcholine level in the striatum was significantly decreased by local application of β-phenylethylamine (10 and 100 μM) in the striatum via a microdialysis probe. The decrease was completely blocked by local co-application of raclopride (10 μM). The β-phenylethylamine-induced decrease in striatal acetylcholine release was not affected by co-perfusion with SCH-23390 (10 μM). These results indicate that systemic administration of β-phenylethylamine increases acetylcholine release, whereas locally applied β-phenylethylamine decreases striatal acetylcholine release in freely moving rats. Furthermore, the dopaminergic system, through the dopamine D₂ receptor, is involved in the locally applied β-phenylethylamine-induced decrease in acetylcholine in the striatum.
Intrastriatal GABA<inf>A</inf> receptor blockade does not alter dopamine D<inf>1</inf>/D<inf>2</inf> receptor interactions in the intact rat striatum
2001, Neuroscience
The purpose of this study was to investigate the effects of intrastriatal blockade of GABA_A receptors on dopamine D₁/D₂ receptor interactions in the intact rat striatum. Muscarinic receptors mediate the ability of the D₂ receptor antagonist, eticlopride, to block an increase in striatonigral neuropeptide messenger RNA stimulated by the full D₁ agonist, SKF-82958. However, because D₂ receptor antagonists activate striatopallidal neurons, it is possible that increased GABA release from local medium spiny axon collaterals also contributes to the ability of eticlopride to block the effects of SKF-82958. This hypothesis was addressed by infusing the GABA_A receptor antagonist, bicuculline, into the dorsal striatum in rats treated with eticlopride and SKF-82958. In contrast to the actions of the muscarinic antagonist, scopolamine, bicuculline did not affect the increase in behaviors induced by SKF-82958 or the ability of eticlopride to block them. Quantitative in situ hybridization demonstrated that bicuculline did not significantly affect basal preprodynorphin messenger RNA, nor did it affect the ability of eticlopride to decrease SKF-82958-induced preprodynorphin messenger RNA. However, the level of the preprodynorphin hybridization signal in bicuculline plus SKF-82958-treated rats was significantly lower than in saline plus SKF-82958-treated rats. In contrast, bicuculline, eticlopride or SKF-82958 by themselves increased basal preproenkephalin messenger RNA. However, there was no significant interaction among bicuculline, eticlopride and SKF-82958 on preproenkephalin messenger RNA levels.
These data indicate that blockade of striatal GABA_A receptors has only a subtle effect on acute dopamine agonist-induced changes in gene expression. These results are discussed in the context of local intrastriatal interactions.

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Modulation of acetylcholine release by D1, D2 dopamine receptors in rat striatum under freely moving conditions

Abstract

Neurosci. Lett.

J. Chromatogr.

Brain Research

Eur. J. Pharmacol.

Neurosci. Lett.

Life Sci.

Eur. J. Pharmacol.

J. Chromatogr.

Brain Research

Life Sci.

Life Sci.

Life Sci.

Eur. J. Pharmacol.

Neurosci. Lett.

Life Sci.

Modulation of acetylcholine release by D₁, D₂ dopamine receptors in rat striatum under freely moving conditions