Dendritic release of dopamine in the substantia nigra

Chéramy, A.; Leviel, Vincent; Głowiński, J.

doi:10.1038/289537a0

Cited by 709 publications

(303 citation statements)

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“…It is well accepted that dopamine is released from the dendrites of dopaminergic neurones in the substantia nigra (Cheramy et al 1981) and can interact with both D2 autoreceptors and with D1 receptors located on the terminals of striato-nigral GABA neurons. It has been reported that when these D1 receptors are stimulated they increase the release of GABA (Flores et al 1993), so that their blockade by SCH23390 will result in a reduction in GABA release.…”

Section: Discussionmentioning

confidence: 99%

Changes in Muscle Tone Are Regulated by D1 and D2 Dopamine Receptors in the Ventral Striatum and D1 Receptors in the Substantia Nigra

Hemsley

Crocker

2001

Neuropsychopharmacology

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Muscle rigidity associated with antipsychotic drug treatment is believed to result from reduced striatal dopamine neurotransmission. In the current study the regulatory roles of dopamine D1 and D2 receptor subfamilies in the dorsal (DSTR) and ventral striatum (VSTR) and substantia nigra (SN) were investigated on muscle tone, assessed as increases in tonic electromyographic (EMG) activity. Rats were injected with the irreversible The use of antipsychotic drugs to treat the symptoms of schizophrenia can be associated with extrapyramidal side effects, which resemble the symptoms of Parkinson's disease and include increased muscle rigidity in up to 40% of patients (Baldessarini and Tarsy 1980). Further, it has been estimated that up to 30% of patients stop taking their medication because of these motor side effects (Hoge et al. 1990). It is not fully understood why antipsychotic drugs, all antagonists at the dopamine D2 receptor (Creese et al. 1976;Seeman et al. 1976; Peroutka and Snyder 1980) produce motor side effects, although there is some early experimental evidence supporting the view that antagonism of D2 receptors in the striatum is important (Chiodo and Bunney 1983;Creese 1983). Findings from studies in humans using positron emission tomography (PET) have led to the concept that a "threshold" of D2 antagonism by antipsychotic drugs of approximately 70%, exists in the striatum, above which patients experience motor side effects (Farde et al. 1992;Nordstrom et al. 1995). Additional support for the striatal D2 threshold hypothesis has N EUROPSYCHOPHARMACOLOGY 2001 -VOL . 25 , NO . 4 Dopamine D1 & D2 Receptors Regulate Muscle Tone 515 been provided by studies using experimental animals Ogren et al. 1994;Alcock and Crocker 1999;Hemsley and Crocker 1999a) and other imaging techniques in humans (Scherer et al. 1994). Further, it has been reported that clozapine, which does not produce motor side effects in humans or animals (Claghorn et al. 1987;Casey 1989), occupies sub-threshold levels of D2 receptors in the striatum (Farde et al. 1992;Hemsley and Crocker 1999a) and substantia nigra (Hemsley and Crocker 1999a). The role of dopamine D1 receptors in the production of motor side effects is unclear, and no relationship to D1 receptor occupancy was shown in PET studies (Farde et al. 1992). However, there is evidence that antagonism of D1 receptors may result in motor side effects Sedvall et al. 1995) and elicit such motor behaviors as catalepsy in rats (Ogren and Fuxe 1988). As many commonly used antipsychotic drugs, such as chlorpromazine, fluphenazine, and clozapine, are also potent dopamine D1 antagonists (Hacksell et al. 1995), it would be useful to understand the contribution that antagonism of the D1 receptor subfamily makes to the production of muscle rigidity.Experimental research investigating the mechanisms underlying the motor side effects associated with the use of antipsychotic drugs has been handicapped by the lack of a relevant, objective, and quantifiable endpoint of extrapyramidal side effects ...

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Section: Discussionmentioning

confidence: 99%

Changes in Muscle Tone Are Regulated by D1 and D2 Dopamine Receptors in the Ventral Striatum and D1 Receptors in the Substantia Nigra

Hemsley

Crocker

2001

Neuropsychopharmacology

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“…In addition, the observation that an amphetamine-inhibiting concentration of MDMA does not significantly attenuate but augments the peak cellular response to cocaine supports the concept that both drugs have similar converging effects blocking DAT. Consequently, during the action of MDMA, DA, normally released from the soma and dendrites of the dopaminergic cells in the extracellular space (Cheramy et al 1981), is not properly cleared by the blocked DAT. Actions similar to those caused by MDMA on the dopaminergic neurons, which are also reserpine-resistant and carbidopa-sensitive, have been described at the neuronal level and said to be caused by the DA uptake blockers cocaine, amineptine, and methylphenidate (Federici et al 2005;Lacey et al 1990;Mercuri et al 1991).…”

Section: Discussionmentioning

confidence: 99%

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Federici

Sebastianelli

Natoli

et al. 2007

Biological Psychiatry

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“…The somatodendritic release of dopamine within substantia nigra is well known (Korf et al, 1976;Chéramy et al, 1981;Robertson et al, 1991;Heeringa and Abercrombie, 1995), and the substantia nigra pars reticulata possesses a density of D 1 receptors that is among the highest of that of any brain region (Savasta et al, 1986;Dawson et al, 1988). Nigral D 1 receptors are localized exclusively on the terminals of the GABAergic striatonigral projection (Porceddu et al, 1986;Yung et al, 1995), and stimulation of these receptors seems to modulate positively the release of GABA from these sites (Floran et al, 1990;C ameron and Williams, 1993).…”

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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Dendritic release of dopamine in the substantia nigra

Cited by 709 publications

References 71 publications

Changes in Muscle Tone Are Regulated by D1 and D2 Dopamine Receptors in the Ventral Striatum and D1 Receptors in the Substantia Nigra

Changes in Muscle Tone Are Regulated by D1 and D2 Dopamine Receptors in the Ventral Striatum and D1 Receptors in the Substantia Nigra

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

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

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Dendritic release of dopamine in the substantia nigra

Cited by 709 publications

References 71 publications

Changes in Muscle Tone Are Regulated by D1 and D2 Dopamine Receptors in the Ventral Striatum and D1 Receptors in the Substantia Nigra

Changes in Muscle Tone Are Regulated by D1 and D2 Dopamine Receptors in the Ventral Striatum and D1 Receptors in the Substantia Nigra

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

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

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