The striatal cholinergic interneuron: Synaptic target of dopaminergic terminals?

Lehmann, John; Langer, S.Z.

doi:10.1016/0306-4522(83)90102-1

Cited by 414 publications

(123 citation statements)

References 120 publications

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“…Dopamine exerts a prominent inhibitory effect on Ach release in the striatum via Drd2 receptors located on striatal cholinergic cells (Bertorelli and Consolo 1990;DeBoer and Abercrombie 1996;Lehmann and Langer 1983;MacKenzie et al, 1989). Consequently, dopaminergic denervation in PD is thought to result in cholinergic hyperactivity with resultant abnormal striatal motor output (Barbeau 1962).…”

Section: Discussionmentioning

confidence: 99%

Motor deficits and altered striatal gene expression in aphakia (ak) mice

et al. 2007

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Like humans with Parkinsons disease (PD), the ak mouse lacks the majority of the substantia nigra pars compacta (SNc) and experiences striatal denervation. The purpose of this study was to test whether motor abnormalities in the ak mouse progress over time, and whether motor function could be associated with temporal alterations in the striatal transcriptome. Ak and wt mice (28 to 180 days old) were tested using paradigms sensitive to nigrostriatal dysfunction. Results were analyzed using a linear mixed model. Ak mice significantly underperformed wt controls in rotarod, balance beam, string test, pole test and cotton shred tests at all ages examined. Motor performance in ak mice remained constant over the first 6 months of life, with the exception of the cotton shred test, in which ak mice exhibited marginal decline in performance. Dorsal striatal semi-quantitative RT-PCR for 19 dopaminergic, cholinergic, glutaminergic and catabolic genes was performed in 1 and 6 month old groups of ak and wt mice. Preproenkephalin levels in ak mice were elevated in both age groups. Drd1, 3 and 4 levels declined over time, in contrast to increasing Drd2 expression. Additional findings included decreased Chrnα6 expression and elevated VGluT1 expression at both time points in ak mice, and elevated AchE expression in young ak mice only. Results confirm that motor ability does not decline significantly for the first 6 months of life in ak mice. Their striatal gene expression patterns are consistent with dopaminergic denervation, and change over time, despite relatively unaltered motor performance.

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Section: Discussionmentioning

confidence: 99%

Motor deficits and altered striatal gene expression in aphakia (ak) mice

et al. 2007

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“…Two distinct dopamine receptors, D 1 and D 2 (C ivelli et al, 1993), are known to participate in this regulation. 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).…”

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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“…Striatal cholinergic signaling is considered to play a central role in motor control as well as in the pathophysiology of different movement disorders such as Parkinson's disease, Huntington's chorea, dystonia, and most recently in progressive supranuclear palsy (Lehmann and Langer, 1983;Albin et al, 2003;Saulle et al, 2004;Warren et al, 2005). Cholinergic interneurons account for a small proportion of the entire striatal neuronal population.…”

Section: Introductionmentioning

confidence: 99%

Endogenous Serotonin Excites Striatal Cholinergic Interneurons via the Activation of 5-HT 2C, 5-HT6, and 5-HT7 Serotonin Receptors: Implications for Extrapyramidal Side Effects of Serotonin Reuptake Inhibitors

Bonsi

Cuomo

Ding³

et al. 2007

Neuropsychopharmacol

123

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The striatum is richly innervated by serotonergic afferents from the raphe nucleus. We explored the effects of this input on striatal cholinergic interneurons from rat brain slices, by means of both conventional intracellular and whole-cell patch-clamp recordings. Bathapplied serotonin (5-HT, 3-300 mM), induced a dose-dependent membrane depolarization and increased the rate of spiking. This effect was mimicked by the 5-HT reuptake blockers citalopram and fluvoxamine. In voltage-clamped neurons, 5-HT induced an inward current, whose reversal potential was close to the K + equilibrium potential. Accordingly, the involvement of K + channels was confirmed either by increasing extracellular K + concentration and by blockade of K + channels with barium. Single-cell reverse transcriptase-polymerase chain reaction (RT-PCR) profiling demonstrated the presence of 5-HT2C, 5-HT6, and 5-HT7 receptor mRNAs in identified cholinergic interneurons. The depolarization/inward current induced by 5-HT was partially mimicked by the 5-HT2 receptor agonist 2,5-dimethoxy-4-iodoamphetamine and antagonized by both ketanserin and the selective 5-HT2C antagonist RS102221, whereas the selective 5-HT3 and 5-HT4 receptor antagonists tropisetron and RS23597-190 had no effect. The depolarizing response to 5-HT was also reduced by the selective 5-HT6 and 5-HT7 receptor antagonists SB258585 and SB269970, respectively, and mimicked by the 5-HT7 agonist, 5-CT. Accordingly, activation of either 5-HT6 or 5-HT7 receptor induced an inward current. The 5-HT response was attenuated by U73122, blocker of phospholipase C, and by SQ22,536, an inhibitor of adenylyl cyclase. These results suggest that 5-HT released by serotonergic fibers originating in the raphe nuclei has a potent excitatory effect on striatal cholinergic interneurons.

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The striatal cholinergic interneuron: Synaptic target of dopaminergic terminals?

Cited by 414 publications

References 120 publications

Motor deficits and altered striatal gene expression in aphakia (ak) mice

Motor deficits and altered striatal gene expression in aphakia (ak) mice

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

Endogenous Serotonin Excites Striatal Cholinergic Interneurons via the Activation of 5-HT 2C, 5-HT6, and 5-HT7 Serotonin Receptors: Implications for Extrapyramidal Side Effects of Serotonin Reuptake Inhibitors

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The striatal cholinergic interneuron: Synaptic target of dopaminergic terminals?

Cited by 414 publications

References 120 publications

Motor deficits and altered striatal gene expression in aphakia (ak) mice

Motor deficits and altered striatal gene expression in aphakia (ak) mice

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

Endogenous Serotonin Excites Striatal Cholinergic Interneurons via the Activation of 5-HT 2C, 5-HT6, and 5-HT7 Serotonin Receptors: Implications for Extrapyramidal Side Effects of Serotonin Reuptake Inhibitors

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