MK‐801 Prevents 1‐Methyl‐4‐Phenyl‐1,2,3,6‐Tetrahydropyridine‐Induced Parkinsonism in Primates

Zuddas, Alessandro; Oberto, Germano; Vaglini, Francesca; Fascetti, Flavia; Fornai, Francesco; Corsini, Giovanni

doi:10.1111/j.1471-4159.1992.tb09429.x

Cited by 151 publications

(55 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These results are in accordance with findings obtained using the non-competitive NMDA antagonist MK-801 in another primate species (Zuddas et al 1992). A neuroprotective effect has been observed at the morphological level, i.e.…”

Section: Discussionsupporting

confidence: 92%

The competitive NMDA antagonist CPP protects substantia nigra neurons from MPTP-induced degeneration in primates

Lange

Löschmann²,

Sofić

et al. 1993

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 92%

The competitive NMDA antagonist CPP protects substantia nigra neurons from MPTP-induced degeneration in primates

Lange

Löschmann²,

Sofić

et al. 1993

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

“…Consistent with this model, rodent studies have demonstrated that lesions of the STN decrease the 6-hydroxydopamine-induced degeneration of SNc neurons (Piallat et al, 1996). Furthermore, N-methyl-D-aspartate antagonists have been found to decrease the 1-methyl-4-phenylpyridiniuminduced degeneration of SNc neurons (Turski et al, 1991) as well as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced degeneration of SNc neurons in primates (Zuddas et al, 1992). Interestingly, direct application of (Ϫ)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK801) in the rat STN has been found to block the 6-hyrdoxydopamine-induced degeneration of SNc neurons (Blandini et al, 2001).…”

Section: Discussionmentioning

confidence: 70%

Group III Metabotropic Glutamate-Receptor-Mediated Modulation of Excitatory Transmission in Rodent Substantia Nigra Pars Compacta Dopamine Neurons

Valenti

Mannaioni²,

Seabrook³

et al. 2005

J Pharmacol Exp Ther

102

View full text Add to dashboard Cite

Glutamate plays an important role in the regulation of dopamine neuron activity. In particular, the glutamatergic input from the subthalamic nucleus is thought to provide control over dopamine neuron firing patterns. The degeneration of dopamine neurons in the substantia nigra pars compacta (SNc) observed in Parkinson's disease (PD) is believed to be due to a complex interplay of factors, including oxidative stress and mitochondrial dysfunction. Although glutamate is not the primary cause of cell death in PD, there is evidence suggesting excessive glutamate release onto dopamine neurons may play a role in continued degeneration. Although many studies have focused on the role of glutamate in the SNc, little work has been directed at exploring the modulatory control of glutamate release in this region. Previous studies have found a high-potency inhibitory effect of nonselective group III mGluR agonist on glutamatergic transmission in the SNc. Using whole-cell patchclamp methods and novel pharmacological tools, we have determined that mGluR4 mediates the group III mGluR modulation of excitatory transmission in the rat SNc. The group III mGluR-selective agonist L-(ϩ)-2-amino-4-phosphonobutyric acid inhibits excitatory transmission in the SNc at low micromolar concentrations with a maximal inhibition occurring at 3 M. This effect was potentiated by the mGluR4-selective allosteric modulator N-phenyl-7-(hydroxymino)cyclopropa [b]chromen-1a-carboxamide and was not mimicked by the mGluR8-selective agonist (S)-3,4-dicarboxyphenylglycine. Interestingly, in an attempt to employ knockout mice to confirm the role of mGluR4, we discovered an apparent species difference suggesting that in mice, both mGluR4 and mGluR8 modulate excitatory transmission in the SNc.

show abstract

“…31,192 The STN is the main excitatory structure of the basal ganglia 151 and has efferences in the SNc. 150 It was originally hypothesized that STN overactivity in PD could contribute to progression of the disease 4,150 and its inactivation may slow or prevent it.…”

Section: Neuroprotectionmentioning

confidence: 99%

Subthalamotomy in the treatment of Parkinson's disease: clinical aspects and mechanisms of action

Jourdain

Schechtmann

Paolo

2014

JNS

View full text Add to dashboard Cite

Parkinson's disease (PD) is a neurodegenerative condition that can be pharmacologically treated with levodopa. However, important motor and nonmotor symptoms appear with its long-term use. The subthalamic nucleus (STN) is known to be involved in the pathophysiology of PD and to contribute to levodopa-induced complications. Surgery is considered in patients who have advanced PD that is refractory to pharmacotherapy and who display disabling dyskinesia. Deep brain stimulation of the STN is currently the main surgical procedure for PD, but lesioning is still performed. This review covers the clinical aspects and complications of subthalamotomy as one of the lesion-based options for PD patients with levodopa-induced dyskinesias. Moreover, the authors discuss the possible effects of subthalamic lesioning.

show abstract

MK‐801 Prevents 1‐Methyl‐4‐Phenyl‐1,2,3,6‐Tetrahydropyridine‐Induced Parkinsonism in Primates

Cited by 151 publications

References 28 publications

The competitive NMDA antagonist CPP protects substantia nigra neurons from MPTP-induced degeneration in primates

The competitive NMDA antagonist CPP protects substantia nigra neurons from MPTP-induced degeneration in primates

Group III Metabotropic Glutamate-Receptor-Mediated Modulation of Excitatory Transmission in Rodent Substantia Nigra Pars Compacta Dopamine Neurons

Subthalamotomy in the treatment of Parkinson's disease: clinical aspects and mechanisms of action

Contact Info

Product

Resources

About