MK801 suppresses the l-DOPA-induced increase of glutamate in striatum of hemi-Parkinson rats

Jonkers, Nadine; Sarre, Sophie; Ebinger, Guy; Michotte, Yvette

doi:10.1016/s0006-8993(01)03147-x

Cited by 79 publications

(70 citation statements)

References 37 publications

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“…In the lesioned side of the striatum of 6-OHDA-leisoned rats, not only did extracellular dopamine levels decrease but also extracellular glutamate levels significantly increased when compared to the intact side of the striatum, which was consistent with previous studies (Calabresi et al, 1993;Meshul et al, 1999;Jonkers et al, 2002). Increased extracellular glutamate in the striatum may contribute to both excitotoxicity of dopaminergic neuron terminals from the SNc and dysfunction of the BG (Hazell et al, 1997).…”

Section: Discussionsupporting

confidence: 90%

Effects of Systemic Administration of Iptakalim on Extracellular Neurotransmitter Levels in the Striatum of Unilateral 6-Hydroxydopamine-Lesioned Rats

Wang

Zhang

et al. 2005

Neuropsychopharmacol

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The function of ATP-sensitive potassium (KATP) channels in nigrostriatal pathway in Parkinson's disease (PD) was studied by employing a novel KATP channel opener iptakalim (Ipt). Apomorphine-induced rotation behavior test and microdialysis experiment were carried out in unilateral 6-hydroxydopamine (6-OHDA) lesioned rats. Behavior test showed that systemic administration of Ipt failed to significantly alleviate apomorphine-induced rotation in unilateral 6-OHDA-lesioned PD model rats. However, using in vivo microdialysis in this PD model rats, it was found that Ipt could increase extracellular dopamine levels in the lesioned side of the striatum and decrease dopamine levels in the intact side of the striatum. Meanwhile, Ipt had no influence on glutamate levels in the intact side, but it did decrease glutamate levels in the lesioned side of the striatum of PD rats. Additionally, in primary cultured rat astrocytes, 6-OHDA decreased overall glutamate uptake activity, but this decrease was recovered and glutamate uptake activity was restored by the opening of KATP channels induced by Ipt and pinacidil. The classical KATP channel blocker glibenclamide completely abolished the effects of Ipt and pinacidil. The present study suggests that (i) the function of KATP channels in the lesioned and intact nigrostriatal pathway is different in unilateral 6-OHDA-lesioned PD model rats. (ii) KATP channels regulate extracellular neurotransmitter levels in the striatum of unilateral 6-OHDAlesioned rats and may play neuroprotective roles due to their effects on glutamate transporters. Neuropsychopharmacology (2006) 31, 933-940.

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Section: Discussionsupporting

confidence: 90%

Effects of Systemic Administration of Iptakalim on Extracellular Neurotransmitter Levels in the Striatum of Unilateral 6-Hydroxydopamine-Lesioned Rats

Wang

Zhang

et al. 2005

Neuropsychopharmacol

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“…Some microdialysis studies (1,4) have reported large increases (þ45% to 146%) in extracellular striatal glutamate after lesion of the nigrostriatal pathway in rats. Acute (4) or repeated (3)L-Dopa administration was also shown to increase extracellular glutamate in the striatum of this model, the reported increase ranging from 224% to about 350% of the basal value.…”

Section: Discussionmentioning

confidence: 99%

Glutamate measurement in Parkinson's disease using MRS at 3 T field strength

et al. 2007

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Loss of nigral dopamine neurons in Parkinson's disease induces abnormal activation of glutamate systems in the basal ganglia. The purpose of this study was to assess these changes in the lentiform nucleus using MRS with optimized glutamate sensitivity (TE-averaged method). Ten patients with Parkinson's disease and 10 healthy controls were examined. Compared with healthy controls, no significant differences in glutamate were measured in patients, but a trend to lower total creatine was observed.

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“…However, the effects of DAdenervation on extracellular striatal GLU levels were reported to be time-dependent. Indeed, Meshul et al (1999) reported biphasic changes, namely increase at 3 weeks (see also Jonkers et al 2002) and decrease at 11 weeks post lesion time. GLU levels in the SNr (You et al 1996) and entopeduncular nucleus (functionally similar to the SNr; Biggs et al 1997) are also increased early (10-14 days) after the lesion.…”

Section: Nmda In Hemiparkinsonian Ratsmentioning

confidence: 93%

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Marti

Mela

Bianchi

et al. 2002

Journal of Neurochemistry

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Dual probe microdialysis was employed in conscious rats to investigate whether endogenous dopamine is involved in the stimulation of glutamate release in the substantia nigra pars reticulata following striatal NMDA receptor activation. Intrastriatal perfusion with NMDA (1 and 10 lM) facilitated nigral glutamate release (dizocilpine-and tetrodotoxin-sensitive). The D 2 dopamine receptor antagonist raclopride increased spontaneous nigral glutamate release and caused a leftward shift in the NMDA sensitivity, lowering NMDA effective concentrations to submicromolar levels. Conversely, the D 1 antagonist SCH23390 prevented the effect of NMDA (1 lM) and caused a rightward shift in the NMDA sensitivity. It was tested whether the antagonist effects were due to dopamine receptor blockade or increased tone on D 1 /D 2 receptors. SCH23390 prevented the raclopride-induced enhancement of spontaneous but not NMDA-evoked glutamate release while raclopride left unchanged the SCH23390-induced inhibition. The physiopathological relevance of the dopaminergic modulation was strengthened by perfusing NMDA in the dopaminedepleted striatum of hemiparkinsonian rats. Nigral glutamate responsiveness to NMDA was enhanced as with raclopride. We conclude that endogenous striatal dopamine regulates both spontaneous and NMDA-induced nigral glutamate release via an opposite control mediated by D 1 facilitatory and D 2 inhibitory receptors. Alterations of this control may subserve the motor symptoms of Parkinson's disease.

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MK801 suppresses the l-DOPA-induced increase of glutamate in striatum of hemi-Parkinson rats

Cited by 79 publications

References 37 publications

Effects of Systemic Administration of Iptakalim on Extracellular Neurotransmitter Levels in the Striatum of Unilateral 6-Hydroxydopamine-Lesioned Rats

Effects of Systemic Administration of Iptakalim on Extracellular Neurotransmitter Levels in the Striatum of Unilateral 6-Hydroxydopamine-Lesioned Rats

Glutamate measurement in Parkinson's disease using MRS at 3 T field strength

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

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MK801 suppresses the l-DOPA-induced increase of glutamate in striatum of hemi-Parkinson rats

Cited by 79 publications

References 37 publications

Effects of Systemic Administration of Iptakalim on Extracellular Neurotransmitter Levels in the Striatum of Unilateral 6-Hydroxydopamine-Lesioned Rats

Effects of Systemic Administration of Iptakalim on Extracellular Neurotransmitter Levels in the Striatum of Unilateral 6-Hydroxydopamine-Lesioned Rats

Glutamate measurement in Parkinson's disease using MRS at 3 T field strength

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D1 and D2 receptors

Contact Info

Product

Resources

About

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors