Modulation of levodopa-induced motor response complications by NMDA antagonists in Parkinson's disease
References (80)
- et al.
The functional anatomy of basal ganglia disorders
Trends in Neuroscience
(1989) - et al.
Excitatory amino acid binding sites in the basal ganglia of the rat: A quantitative autoradiographic study
Neuroscience
(1992) - et al.
The distribution of excitatory amino acid receptors in the normal human midbrain and basal ganglia with implications for Parkinson's disease: A quantitative autoradiographic study using [3H]MK-801, [3H]glycine, [3H]CNQX and [3H]kainate
Brain Research
(1994) - et al.
MK-801 reverses effects of chronic levodopa and D1 and D2 dopamine agonist-induced rotational behavior
Brain Research
(1995) - et al.
Dextromethorphan and parkinsonism
Lancet
(1992) - et al.
Anti-parkinsonian effects of EAA antagonists in the entopeduncular nucleus are due to an action at NMDA-like receptors
European Journal of Pharmacology
(1990) - et al.
Modulatory functions of neurotransmitters in the striatum: ACh/dopamine/NMDA interactions
Trends in Neuroscience
(1994) - et al.
Continuous and intermittent levodopa differentially affect rotation induced by D-1 and D-2 dopamine agonists
European Journal of Pharmacology
(1989) - et al.
Excitatory amino acid receptor antagonists modify regional cerebral metabolic responses to levodopa in 6-hydroxydopamine-lesioned rats
Neuroscience
(1994) - et al.
Combined treatment of parkinsonism with l-dopa and amantadine
Lancet
(1970)
Antiparkinsonian action of dextromethorphan in the reserpine-treated mouse
European Journal of Pharmacology
Apomorphine-induced changes in striatal and pallidal neuronal activity are modified by NMDA and muscarinic receptor blockade
Life Sciences
Postsynaptic integration of glutamatergic and dopaminergic signals in the striatum
Progress in Neurobiology
Ligand affinities at recombinant N-methyl-d-aspartate receptors depend on subunit composition
European Journal of Pharmacology [Molecular Pharmacology Section]
Effect on parkinsonian signs and symptoms of bilateral subthalamic nucleus stimulation
Lancet
Chronic administration of NMDA antagonists induces D2 receptor synthesis in rat striatum
Molecular Brain Research
Neural mechanisms underlying parkinsonian symptoms based upon regional uptake of 2-deoxyglucose in monkeys exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Neuroscience
l-[3H]Glutamate binds to kainate-, NMDA- and AMPA-sensitive binding sites: an autoradiographic analysis
Brain Research
MK-801 potentiates dopaminergic D1 but reduces D2 responses in the 6-hydroxydopamine model of Parkinson's disease
European Journal of Pharmacology
Motor fluctuations in levodopa treated parkinsonian rats: relation to lesion extent and treatment duration
Brain Research
D2 dopamine receptor messenger RNA is altered to a greater extent by blockade of glutamate receptors than by blockade of dopamine receptors
Neuroscience
Dyskinesia in the primate following injection of an excitatory amino acid antagonist into the medial segment of the globus pallidus
Brain Research
Neurons of the subthalamic nucleus in primates display glutamate but not GABA immunoreactivity
Brain Research
Facilitation of dopamine D1 receptor-but not dopamine receptor-dependent locomotion by glutamate antagonists in the reserpine-treated mouse
European Journal of Pharmacology
NBQX (6-nitro-sulfamoyl-benzo-quinoxaline-dione) and CPP (3-carboxy-piperazin-propyl phosphonic acid) potentiate dopamine agonist induced rotations in substantia nigra lesioned rats
Neuroscience Letters
The competitive NMDA antagonist CGP40.116 enhances L-DOPA response in MPTP-treated marmosets
Neuropharmacology
Adverse clinical side effects of levodopa therapy
Role of selective D1 and D2 agonists in inducing dyskinesia in drug-naive MPTP monkeys
Reversal of experimental parkinsonism by lesions of the subthalamic nucleus
Science
Parkinson's disease and long-term levodopa therapy
Continuous administration decreases and pulsatile administration increases behavioral sensitivity to a novel dopamine D-2 agonist (U-91356A) in MPTP monkeys
Journal of Pharmacology and Experimental Therapeutics
Dyskinesia and wearing-off following dopamine D1 receptor agonist treatment in drug-naive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned primates
Movement Disorders
Acute pharmacologic blockade of dyskinesias in Parkinson's disease
Movement Disorders
Does levodopa aggravate Parkinson's disease?
Neurology
Influence of previous exposure to levodopa on the interaction between dizocilpine and dopamine D1 and D2 agonists in rats with 6-hydroxydopamine-induced lesions
Journal of Pharmacology and Experimental Therapeutics
Wearing-off fluctuations in Parkinson's disease: contribution of postsynaptic mechanisms
Annals of Neurology
Amantadine sulphate in treating Parkinson's disease: clinical effects, psychometric tests and serum concentrations
Journal of Neurology
Alleviation of parkinsonism by antagonism of excitatory amino acid transmission in the medial segment of the globus pallidus in rat and primate
Movement Disorders
The molecular basis of NMDA receptor subtypes: Native receptor diversity is predicted by subunit composition
Journal of Neuroscience
Neuromodulatory actions of dopamine in the neostriatum are dependent upon the excitatory amino acid receptor sybtypes activated
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Principles and Practice of Movement Disorders
2021, Principles and Practice of Movement DisordersAnti-NMDA Receptor Encephalitis: Clinical Features and Basic Mechanisms
2018, Advances in PharmacologyCitation Excerpt :In addition, NMDA knockdown in mice leads to hypoventilation, the cause of death in many patients with anti-NMDARE (Forrest et al., 1994). Finally, NMDAR modulation is linked to control of dyskinesias, an aspect that could be associated with the prominent dyskinesia in anti-NMDARE (Blanchet, Papa, Metman, Mouradian, & Chase, 1997). Thus, studies identifying NMDARs as the autoantigen in this disorder are consistent with the expected features of dysfunctional NMDARs.
Dyskinesias and impulse control disorders in Parkinson's disease: From pathogenesis to potential therapeutic approaches
2015, Neuroscience and Biobehavioral ReviewsChronic treatment with MPEP, an mGlu5 receptor antagonist, normalizes basal ganglia glutamate neurotransmission in L-DOPA-treated parkinsonian monkeys
2013, NeuropharmacologyCitation Excerpt :Hence, this evidence strongly suggests that NMDA receptors containing NR2B subunits are involved in the pathophysiology of LID and might contribute to their development. Although less receptor specific, dextrorphan, dextromethorphan and amantadine, known to block NMDA receptors, also show antidyskinetic activity in humans (Blanchet et al., 1996, 1997; Luginger et al., 2000; Metman et al., 1999; Rajput et al., 1998; Ruzicka et al., 2000; Snow et al., 2000; Verhagen Metman et al., 1998a). The role of AMPA receptors in LID is also supported by reports of improved LID with blockade of AMPA receptors in the MPTP monkey model (Bibbiani et al., 2005; Konitsiotis et al., 2000).
Intermittent Dopaminergic Stimulation causes Behavioral Sensitization in the Addicted Brain and Parkinsonism
2009, International Review of NeurobiologyCitation Excerpt :Moreover, l-DOPA alters gene expression-related neuronal phenotype for striatal glutamatergic transmission (Chase and Oh, 2000; Oh and Chase, 2002), both affecting NMDA (Oh et al., 1999) and non-NMDA (Marin et al., 2000) glutamate receptor subunits. This mechanism has been implicated in motor sensitization leading to dyskinesia as demonstrated by blocking NMDA (Blanchet et al., 1997) or AMPA (Konitsiotis et al., 2000) glutamate receptors to reduce l-DOPA-induced dyskinesia. These findings extended the role of glutamate antagonists from preventing the pathogenesis of PD to the treatment of drug-induced motor complications (Fornai et al., 1996, 1997; Zuddas et al., 1992).
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Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bldg 10, Rm 5C103, 10 Center Drive MSC 1406, Bethesda, MD 20892-1406, USA.