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D1 and D2 dopamine receptor-regulated gene expression of striatonigral and striatopallidal neurons.
TLDR
The differential effects of dopamine on striatonigral and striatopallidal neurons are mediated by their specific expression of D1 and D2 dopamine receptor subtypes, respectively.
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Striatal dopamine- and glutamate-mediated dysregulation in experimental parkinsonism
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Enhanced tyrosine phosphorylation of striatal NMDA receptor subunits: effect of dopaminergic denervation and l-DOPA administration
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Differing effects of N-methyl-D-aspartate receptor subtype selective antagonists on dyskinesias in levodopa-treated 1-methyl-4-phenyl-tetrahydropyridine monkeys.
TLDR
The data suggest that the NR2 subunit selectivity profile of NMDA receptor antagonists can play an important role in predicting behavioral outcome and offer more evidence that NR2B-selective NMda receptor antagonists may be useful agents in the treatment of Parkinson's disease.
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Serotonin 5-HT1A agonist improves motor complications in rodent and primate parkinsonian models
TLDR
Drugs acting to stimulate 5-HT1A receptors could prove useful in the treatment of the motor response complications in parkinsonian patients.
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Amantadine reduces levodopa‐induced dyskinesias in parkinsonian monkeys
TLDR
Results lend support to the view that glutamate receptormediated mechanisms contribute to levodopa‐induced dyskinesias and suggest that amantadine could alleviate such complications in parkinsonian patients, especially with careful dose optimization.
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Striatal mechanisms and pathogenesis of parkinsonian signs and motor complications.
TLDR
Observations that NMDA receptor antagonists injected into the striatum or given systemically have the ability to act palliatively or prophylactically to alleviate levodopa-induced response alterations support the view that sensitization of striatal NMDA receptors contributes to the pathogenesis of motor dysfunction in Parkinson's disease.
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Combined blockade of AMPA and NMDA glutamate receptors reduces levodopa-induced motor complications in animal models of PD
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D1 dopamine receptor activation required for postsynaptic expression of D2 agonist effects.
TLDR
The previously held view that D2 receptors alone are responsible for evoking the changes in behavior and basal ganglia output induced by nonselective dopamine agonists and endogenous dopamine is not supported by these results, which indicate that these phenomena require concurrent stimulation of both dopamine receptor subtypes.
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Motor fluctuations in levodopa treated parkinsonian rats: relation to lesion extent and treatment duration
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