Subthalamic nucleus modulates burst firing of nigral dopamine neurones via NMDA receptors

Chergui, Karima; Akaoka, H.; Charléty, P. J.; Saunier, C; Buda, M.; Chouvet, Guy

doi:10.1097/00001756-199406020-00006

Cited by 110 publications

(60 citation statements)

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“…Pharmacological activation of the subthalamic nucleus by bicuculline infusion led to an initial decrease in firing rate and the incidence of burst firing with the opposite biphasic effects following inactivation of the subthalamic nucleus with muscimol (Smith and Grace 1992). In another study, local infusions of GABA or bicuculline into subthalamic nucleus produced decreases and increases in firing rate and burst firing in nigral dopaminergic neurons, but these effects were observed in only about half of the neurons, with the other half showing the opposite effects (Chergui et al 1994).…”

Section: Glutamatergic Afferentsmentioning

confidence: 94%

Electrophysiological Pharmacology of Mesencephalic Dopaminergic Neurons

Diana¹,

Tepper²

2002

Dopamine in the CNS II

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Section: Glutamatergic Afferentsmentioning

confidence: 94%

Electrophysiological Pharmacology of Mesencephalic Dopaminergic Neurons

Diana¹,

Tepper²

2002

Dopamine in the CNS II

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“…hippocampus and prefrontal cortex) and subcortical (laterodorsal tegmental and pedunculopontine tegmental nuclei, the bed nucleus of the stria terminalis and the superior colliculus) brain regions (Morikawa and Paladini, 2011). Activation of NMDARs in the VTA increases DA neuron burst firing rates (Overton and Clark, 1992;Chergui et al, 1993), whereas NMDAR antagonists decrease spontaneous bursts of VTA DAergic neurons after the activation of glutamatergic inputs to the VTA Clark, 1992, 1997;Chergui et al, 1994;Morikawa and Paladini, 2011). In a similar fashion, in mutant mice lacking NMDARs specifically on DAergic neurons, burst firing of VTA DAergic neurons and striatal DA release are attenuated after electrical stimulation of the pedunculopontine tegmental nucleus, which projects glutamatergic inputs to the VTA (Zweifel et al, 2009).…”

Section: Lack Of Direct Effects Of Ketamine On Daergic Functionmentioning

confidence: 99%

Effects of Ketamine and Ketamine Metabolites on Evoked Striatal Dopamine Release, Dopamine Receptors, and Monoamine Transporters

Can

Zanos

Moaddel³

et al. 2016

Journal of Pharmacology and Experimental Therapeutics

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Following administration at subanesthetic doses, (R,S)-ketamine (ketamine) induces rapid and robust relief from symptoms of depression in treatment-refractory depressed patients. Previous studies suggest that ketamine's antidepressant properties involve enhancement of dopamine (DA) neurotransmission. Ketamine is rapidly metabolized to (2S,6S)-and (2R,6R)-hydroxynorketamine (HNK), which have antidepressant actions independent of Nmethyl-D-aspartate glutamate receptor inhibition. These antidepressant actions of (2S,6S;2R,6R)-HNK, or other metabolites, as well as ketamine's side effects, including abuse potential, may be related to direct effects on components of the dopaminergic (DAergic) system. Here, brain and blood distribution/clearance and pharmacodynamic analyses at DA receptors (D 1 -D 5 ) and the DA, norepinephrine, and serotonin transporters were assessed for ketamine and its major metabolites (norketamine, dehydronorketamine, and HNKs). Additionally, we measured electrically evoked mesolimbic DA release and decay using fast-scan cyclic voltammetry following acute administration of subanesthetic doses of ketamine (2, 10, and 50 mg/kg, i.p.). Following ketamine injection, ketamine, norketamine, and multiple hydroxynorketamines were detected in the plasma and brain of mice. Dehydronorketamine was detectable in plasma, but concentrations were below detectable limits in the brain. Ketamine did not alter the magnitude or kinetics of evoked DA release in the nucleus accumbens in anesthetized mice. Neither ketamine's enantiomers nor its metabolites had affinity for DA receptors or the DA, noradrenaline, and serotonin transporters (up to 10 mM). These results suggest that neither the side effects nor antidepressant actions of ketamine or ketamine metabolites are associated with direct effects on mesolimbic DAergic neurotransmission. Previously observed in vivo changes in DAergic neurotransmission following ketamine administration are likely indirect.

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“…One model of DA function posits that the mesolimbic DA system is regulated via two independent mechanisms: (1) transient or "phasic" DA release driven by DA neuron burst firing and (2) extrasynaptic or "tonic" levels DA dependent on basal DA neuron activity and regulated via presynaptic inputs (Grace, 1991;Floresco et al, 2003). DA neuron burst firing induces a large transient increase in perisynaptic DA (Chergui et al, 1994) and is considered to be the functionally relevant signal that encodes reward prediction or incentive salience (Berridge and Robinson, 1998;Schultz, 1998), whereas tonic DA transmission occurs on a much slower scale and is proposed to set the background level of DA system activation (Grace, 1991).…”

Section: Introductionmentioning

confidence: 99%

Aberrant Hippocampal Activity Underlies the Dopamine Dysregulation in an Animal Model of Schizophrenia

2007

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Evidence supports a dysregulation of subcortical dopamine (DA) system function as a common etiology of psychosis; however, the factors responsible for this aberrant DA system responsivity have not been delineated. Here, we demonstrate in an animal model of schizophrenia that a pathologically enhanced drive from the ventral hippocampus (vHipp) can result in aberrant dopamine neuron signaling. Adult rats in which development was disrupted by prenatal methylazoxymethanol acetate (MAM) administration display a significantly greater number of spontaneously firing ventral tegmental DA neurons. This appears to be a consequence of excessive hippocampal activity because, in MAM-treated rats, vHipp inactivation completely reversed the elevated DA neuron population activity and also normalized the augmented amphetamine-induced locomotor behavior. These data provide a direct link between hippocampal dysfunction and the hyper-responsivity of the DA system that is believed to underlie the augmented response to amphetamine in animal models and psychosis in schizophrenia patients.

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Subthalamic nucleus modulates burst firing of nigral dopamine neurones via NMDA receptors

Cited by 110 publications

References 0 publications

Electrophysiological Pharmacology of Mesencephalic Dopaminergic Neurons

Electrophysiological Pharmacology of Mesencephalic Dopaminergic Neurons

Effects of Ketamine and Ketamine Metabolites on Evoked Striatal Dopamine Release, Dopamine Receptors, and Monoamine Transporters

Aberrant Hippocampal Activity Underlies the Dopamine Dysregulation in an Animal Model of Schizophrenia

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