Cholinergic-dopaminergic interaction in the striatum: The effect of 6-hydroxydopamine or pimozide treatment on the increased striatal acetylcholine levels induced by apomorphine, piribedil andD-amphetamine

Ladinsky, H.; Consolo, S.; Bianchi, S.; Samanin, R.; Ghezzi, D.

doi:10.1016/0006-8993(75)90977-4

Cited by 95 publications

(11 citation statements)

References 19 publications

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“…The D 2 receptor inhibits striatal acetylcholine (ACh) efflux (Lehmann and Langer, 1983;, whereas the D 1 receptor modulates this variable in an excitatory manner (Fage and Scatton, 1986;Consolo et al 1987;Damsma et al, 1990;Imperato et al, 1993). Thus, indirect dopamine agonists such as amphetamine have been observed to produce an increase, a decrease, or no net change in striatal ACh efflux depending on the dose administered and according to the methods used in the experiment (Ladinsky et al, 1975;DeBoer and Abercrombie, 1996a). Such variability in ACh response to mixed dopaminergic agonists presumably reflects the fact that D 2 -mediated inhibition or D 1 -mediated excitation may predominate in determining the level of ACh output in any given circumstance and that the effects of the two influences may even cancel.…”

Section: Dopamine D 1 Receptor; In Vivo Microdialysismentioning

confidence: 99%

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Abercrombie

Deboer

1997

J. Neurosci.

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Dopamine release can regulate striatal acetylcholine efflux in vivo through at least two receptor mechanisms: (1) direct inhibition by dopamine D 2 receptors on the cholinergic neurons, and (2) excitation initiated by dopamine D 1 receptors. The neuroanatomical locus of the latter population of D 1 receptors and the pathway(s) involved in the expression of their influence are controversial issues. We have tested the hypothesis that D 1 receptors in substantia nigra pars reticulata are involved in the excitatory component of dopaminergic actions on striatal acetylcholine output. In vivo microdialysis was used in awake rats. Infusion of the selective D 1 receptor agonist R(ϩ)-1-Phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol (SKF 38393) hydrochloride into pars reticulata of substantia nigra elicited a significant increase in striatal acetylcholine efflux. Likewise, D-amphetamine applied into pars reticulata of substantia nigra by reverse dialysis produced an elevation in acetylcholine output measured at a second microdialysis probe in the striatum. Application of D-amphetamine in the striatum by reverse dialysis elicited a decrease in striatal acetylcholine efflux that could be reversed subsequently by local application of Damphetamine in substantia nigra pars reticulata. A 2 mg/kg intraperitoneal dose of D-amphetamine, which has no net effect on striatal acetylcholine output under control conditions, elicited a significant decrease in acetylcholine efflux when the D 1 receptor antagonist R(ϩ)-7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine (SCH 23390) hydrochloride was applied simultaneously via a second microdialysis probe in substantia nigra pars reticulata. Thus, an excitatory D 1 -mediated influence on striatal acetylcholine output is initiated in substantia nigra pars reticulata, and this influence contributes to the effects of indirect dopaminergic agonists such as D-amphetamine on striatal acetylcholine efflux. These results indicate an important role of somatodendritic dopamine release, in addition to nerve terminal dopamine release, in the regulation of activity in basal ganglia circuits.

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Section: Dopamine D 1 Receptor; In Vivo Microdialysismentioning

confidence: 99%

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Abercrombie

Deboer

1997

J. Neurosci.

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“…On the basis of data obtained in the 1970s, systemically administered d-amphetamine was considered to inhibit acetylcholine (ACh) release in the striatum. Specifically, given the fact that high doses of d-amphetamine increase striatal tissue concentrations of ACh, it was hypothesized that such increases reflect a reduction in the synaptic release of ACh, with this leading to an accumulation of the transmitter intraneuronally (Consolo et al, 1974;Sethy and Van Woert, 1974;Agid et al, 1975;Ladinsky et al, 1975). On the same grounds, it was concluded that stimulation of dopamine (DA) D2 receptors inhibits (Consolo et al, , 1987Wong et a!., 1983), whereas stimulation of D1 receptors enhances, striatal ACh neurotransmission (Fage and Scatton, 1986;Consolo et al, 1987).…”

mentioning

confidence: 99%

Dopaminergic Regulation of Striatal Acetylcholine Release: The Critical Role of Acetylcholinesterase Inhibition

Acquas

Fibiger

1998

Journal of Neurochemistry

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This study examined the effects of different levels of acetylcholinesterase (AChE) inhibition on dopaminergic regulation of striatal acetylcholine (ACh) release as estimated by in vivo brain microdialysis. Systemic administration of d‐amphetamine (2 or 10 mg/kg) increased the striatal output of ACh when the AChE inhibitor neostigmine (0.1 µM) was present in the perfusion fluid. In contrast, when the same experiments were conducted at 0.01 µM neostigmine, d‐amphetamine failed to affect (2 mg/kg) or significantly decreased (10 mg/kg) striatal ACh output. The inhibitory action of the D2 receptor agonist quinpirole (0.2 mg/kg) was significantly greater at 0.01 µM than at 0.1 µM neostigmine. Similarly, there was a nonsignificant trend for the D2 antagonist raclopride (1 mg/kg) to stimulate ACh release to a greater extent at the low neostigmine concentration. In contrast, the stimulant effects of systemic administration of the D1 agonist A‐77636 (1.46 mg/kg) on striatal ACh release were the same at the two neostigmine concentrations. These results demonstrate that the concentration of an AChE inhibitor in the perfusion solution can quantitatively and even qualitatively influence the manner in which dopaminergic agents regulate ACh overflow in the striatum. On comparing the present results with earlier reports concerning the effects of d‐amphetamine on tissue concentrations of ACh, it is tentatively concluded that a low neostigmine concentration is the more physiologically relevant condition. Under such conditions, at moderate doses d‐amphetamine does not appear to alter striatal ACh release, with this likely being due to the opposing actions of D1 and D2 receptors. Nevertheless, until the endogenous interstitial concentrations of striatal ACh can be measured by other methods, the physiological relevance of ACh microdialysis studies in the striatum will remain uncertain.

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“…Neuroleptic drugs, by blocking dopaminergic receptors, seem to remove a tonic inhibition of the intrinsic cholinergic neurons in the striatum (Connor, 1970; Bunney et al, 1973) by increasing their activity. This is demonstrated by the enhancement of acetylcholine (ACh) output from the striatum following the administration of chlorpromazine in cats (Stadler et al, 1973), by the decrease in striatal ACh levels (Ladinsky et al, 1974;Sethy and Van Woert, 1974), and by the stimulation of striatal ACh turnover rate after a single administration of chlorpromazine or haloperidol (Trabucchi et al, 1974). Repeated administration of neuroleptics induces tolerance: catalepsy tends to disappear, ACh levels return to normal (Sethy, 1976) or even show an increase (Consolo et al, 1978), and the stimulation of striatal ACh turnover rate disappears .…”

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confidence: 99%

Choline High‐Affinity Uptake and Metabolism and Choline Acetyltransferase Activity in the Striatum of Rats Chronically Treated with Neuroleptics

Pedata

Sorbi

Pepeu

1980

Journal of Neurochemistry

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High-affinity uptake of choline and choline acetyltransferase activity (ChAT) were measured in the striatum of rats treated for 45-60 days with haloperidol (1 mg/kg per os) and pimozide (1 mg/kg per os) daily and with fluspirilene (1 mg/kg i.m.) twice a week. Haloperidol and fluspirilene caused a 20%, and pimozide a 38%, increase in high-affinity uptake of choline. They also caused a significant decrease in ChAT activity: haloperidol, 20%; pimozide, 27%; and fluspirilene, 42%. In rats treated with fluspirilene for 65-80 days the metabolism of [3H] choline taken up by striatal synaptosomes was investigated. A 33% increase in total radioactivity, a significant increase in labelled acetylcholine (ACh), a relative decrease in labelled choline, and no change in labelled phosphorylcholine and betaine were found. It is concluded that the increase in high-affinity choline uptake caused by chronic administration of neuroleptic drugs is associated with a parallel increase in choline utilization for ACh formation. On the other hand, the decrease in ChAT activity does not appear to influence ACh formation.

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Cholinergic-dopaminergic interaction in the striatum: The effect of 6-hydroxydopamine or pimozide treatment on the increased striatal acetylcholine levels induced by apomorphine, piribedil andD-amphetamine

Cited by 95 publications

References 19 publications

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Dopaminergic Regulation of Striatal Acetylcholine Release: The Critical Role of Acetylcholinesterase Inhibition

Choline High‐Affinity Uptake and Metabolism and Choline Acetyltransferase Activity in the Striatum of Rats Chronically Treated with Neuroleptics

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Cholinergic-dopaminergic interaction in the striatum: The effect of 6-hydroxydopamine or pimozide treatment on the increased striatal acetylcholine levels induced by apomorphine, piribedil andD-amphetamine

Cited by 95 publications

References 19 publications

Substantia Nigra D1Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Substantia Nigra D1Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Dopaminergic Regulation of Striatal Acetylcholine Release: The Critical Role of Acetylcholinesterase Inhibition

Choline High‐Affinity Uptake and Metabolism and Choline Acetyltransferase Activity in the Striatum of Rats Chronically Treated with Neuroleptics

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Product

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Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism