Differential effects of activating D1 and D2 receptors on electrophysiology of neostriatal neurons in a rat model of Parkinson's disease induced by paraquat and maneb

Xu, Huamin; Chen, Ruirui; Cai, Xiao-Yan; He, Defu

doi:10.1016/j.neures.2011.08.011

Cited by 9 publications

(4 citation statements)

References 68 publications

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“…This reasoning is consistent with Liang et al ( 2008 ) who reported that in awake MPTP-lesioned monkeys, L-dopa excited a subgroup of SPNs that were presumed to be dSPNs and inhibited a subgroup of SPNs that were presumed to be iSPNs (Liang et al, 2008 ). However, some anesthetized results show an increased activity of SPNs after DA depletion in rats reportedly reduced by D1 agonists, and increased further by D2 agonists (Tseng et al, 2004 ; Xu et al, 2011 ); such data complicates interpretations arising from the canonical model. Our data–especially given such low identified cell numbers–do not exclude the possibility that D1 agonist may decrease the activity of D1R-expressing (or D2R-expressing) SPNs; further research may shed more light here and somehow expand the scope of the canonical model (e.g., Cui et al, 2013 ; Sippy et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Hyperactive Response of Direct Pathway Striatal Projection Neurons to L-dopa and D1 Agonism in Freely Moving Parkinsonian Mice

Sagot

Zhou

2018

Front. Neural Circuits

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Dopamine (DA) profoundly stimulates motor function as demonstrated by the hypokinetic motor symptoms in Parkinson's disease (PD) and by the hyperkinetic motor side effects during dopaminergic treatment of PD. Dopamine (DA) receptor-bypassing, optogenetics- and chemogenetics-induced spike firing of striatal DA D1 receptor (D1R)-expressing, direct pathway medium spiny neurons (dSPNs or dMSNs) promotes movements. However, the endogenous D1R-mediated effects, let alone those of DA replacement, on dSPN spike activity in freely-moving animals is not established. Here we show that using transcription factor Pitx3 null mutant (Pitx3Null) mice as a model for severe and consistent DA denervation in the dorsal striatum in Parkinson's disease, antidromically identified striatonigral neurons (D1R-expressing dSPNs) had a lower baseline spike firing rate than that in DA-intact normal mice, and these neurons increased their spike firing more strongly in Pitx3Null mice than in WT mice in response to injection of L-dopa or the D1R agonist, SKF81297; the increase in spike firing temporally coincided with the motor-stimulating effects of L-dopa and SKF81297. Taken together, these results provide the first evidence from freely moving animals that in parkinsonian striatum, identified behavior-promoting dSPNs become hyperactive upon the administration of L-dopa or a D1 agonist, likely contributing to the profound dopaminergic motor stimulation in parkinsonian animals and PD patients.

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Section: Discussionmentioning

confidence: 99%

Hyperactive Response of Direct Pathway Striatal Projection Neurons to L-dopa and D1 Agonism in Freely Moving Parkinsonian Mice

Sagot

Zhou

2018

Front. Neural Circuits

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“…It might be the case that the population rate of fast‐spiking neurons is higher than that estimated by anatomical evidence, because the diameter of fast‐spiking neurons is slightly larger than that of MS neurons (17 μm vs. 13 μm; Kawaguchi, ). In the dorsal striatum, the firing frequency of the MS neurons is increased and decreased by D 1 ‐ and D 2 ‐like receptor agonists, respectively (Bamford et al, ; Xu et al, ). This idea may explain the underlying mechanisms of the present results of the divergent apomorphine‐induced effects on the PA neuronal activities.…”

Section: Discussionmentioning

confidence: 99%

Apomorphine‐induced modulation of neural activities in the ventrolateral striatum of rats

Fujita¹,

Kato

Cui

et al. 2013

Synapse

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The dopaminergic system in the ventrolateral portion of the striatum (Svl), part of the basal ganglia, regulates orofacial movements; bilateral co-stimulation of both dopamine D1 -like and D2 -like receptors elicits repetitive jaw movements in rats. However, how the activities of Svl neurons are modulated by the activation of dopaminergic receptors remains unknown. We systematically injected apomorphine, a non-selective dopamine receptor agonist that induced jaw movements under urethane anesthesia, and performed multi-channel unit recording from Svl neurons. The Svl neurons were classified into two subgroups: (1) the phasically active (PA) neurons represented by mainly the medium spiny neurons and the GABAergic interneurons in part, and (2) the tonically active (TA) neurons composed of mainly the cholinergic interneurons. Apomorphine modulated PA neuron firing frequency with wide variability; 33.3% of the PA neurons were facilitated, while 38.3% were suppressed. In the majority of TA neurons, the firing frequency was reduced by apomorphine (71.1%). The cross-correlations between PA and PA, PA and TA, and TA and TA neurons were analyzed, and pairs of PA neurons and pairs of PA and TA neurons, showed negligible apomorphine-induced effect on the number of synchronized spikes. In contrast, pairs between TA neurons showed a consistent decrease in the number of synchronized spikes. The apomorphine-induced suppression of TA neuron activities with decreased synchronized outputs is likely to reduce the amount of locally released acetylcholine, which may contribute to the induction of apomorphine-induced jaw movements in rats.

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“…Systemic administration of SKF 38393 did not differ from SKF 81297 in terms of rescuing elecotrophysiological metrics after DA-depletion (Tseng et al, 2004), and it resulted homogeneously in increases (both in-\significant) having no obvious baseline correlation in WT animals. (Xu et al, 2011) (Results from these last two studies are also noteworthy for their opposing results when D1 agonist was given to DA deficient animals; Tseng et al, 2004 found that SKF-81297 decreased spiking, whereas Xu et al, 2011 found a statistically insignificant increase; thus expectations for Pitx3Null dorsal SPNs responses to D1 agonist are less clear. )…”

Section: D1 Agonist Skf 81297mentioning

confidence: 99%

“…In another example, strict application of SKF-81297 in a similar setting for dorsal striatum showed no obvious correlation with baseline for polarity or intensity. (Xu et al, 2011) Finally, Delfino et al, 2007, found that motor cortical activity was enhanced in hemi-lesioned rats having their BOLD response measured, suggesting that motor network glutamatergic striatal input plays a larger role in the D1 agonist response than in the l-DOPA response for WT. Thus expectations are that high-rate non-dorsal SPNs in WT may tend to decrease in rate albeit after drug during locomotor increases, significant or not, and any dorsal baseline correlation should be weak, if present at all.…”

Section: Genotype Differencesmentioning

confidence: 99%

Pitx3Null Mutant (Striatal Dopamine-Deficient) Mice Have Exaggerated Spiny Projection Neuron Responses to l-DOPA and D1 Agonism and Lack Baseline Striatonigral Spiking

Abidi¹

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Differential effects of activating D1 and D2 receptors on electrophysiology of neostriatal neurons in a rat model of Parkinson's disease induced by paraquat and maneb

Cited by 9 publications

References 68 publications

Hyperactive Response of Direct Pathway Striatal Projection Neurons to L-dopa and D1 Agonism in Freely Moving Parkinsonian Mice

Hyperactive Response of Direct Pathway Striatal Projection Neurons to L-dopa and D1 Agonism in Freely Moving Parkinsonian Mice

Apomorphine‐induced modulation of neural activities in the ventrolateral striatum of rats

Pitx3Null Mutant (Striatal Dopamine-Deficient) Mice Have Exaggerated Spiny Projection Neuron Responses to l-DOPA and D1 Agonism and Lack Baseline Striatonigral Spiking

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