Two-methyl-6-phenylethynyl-pyridine (MPEP), a metabotropic glutamate receptor 5 antagonist, with low doses of MK801 and diazepam: A novel approach for controlling status epilepticus

Dynamic Changes in Striatal mGluR1 But Not mGluR5 during Pathological Progression of Parkinson's Disease in Human Alpha-SynucleinA53TTransgenic Rats: A Multi-PET Imaging Study

“…11 C]ABP688 and [ 18 F]FE-PE2I, kinetic analyses were performed according to the SRTM using TACs obtained from the cerebellum as a reference tissue (Elmenhorst et al, 2010;Sasaki et al, 2012). Respective parametric images were scaled according to the BP ND and reconstructed using PMOD software and the TACs acquired from reference regions.…”

“…Moreover, in acute PD models using 6-hydroxy dopamine (6-OHDA) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, mGluR1 or mGluR5 antagonist administration protected against dopaminergic neuronal loss in the substantia nigra (Aguirre et al, 2001;Vernon et al, 2007). Additionally, in a 6-OHDA-treated nonhuman primate acute PD model, mGluR5 expression was elevated in the striatum, whereas mGluR1 expression was decreased in the globus pallidus and substantia nigra (Kaneda et al, 2005;Samadi et al, 2008;Sanchez-Pernaute et al, 2008). These findings suggest that alterations in group I mGluR expression are associated with the onset of PD.…”

“…Among the glutamate receptor family, metabotropic glutamate receptors are G-protein-coupled receptors comprising eight subtypes (mGluR1-mGluR8). These subtypes are divided into three groups (groups I-III), based on differences in the G-protein ␣ subunit and subsequent transduction pathways (Nakanishi et al, 1998). The receptor subtypes mGluR1 and mGluR5 are members of group I, and activate the G q -protein.…”

“…A number of reports have demonstrated that mGluR1 and mGluR5 modulators provided neuroprotection in CNS disorders such as stroke (Bao et al, 2001;Kohara et al, 2008), Huntington's disease (Schiefer et al, 2004), AD (Ulus and Wurtman, 1997), epilepsy (Löscher et al, 2006;Tang et al, 2007), and PD (Dekundy et al, 2006;Vernon et al, 2008;De Leonibus et al, 2009;Rylander et al, 2010). Moreover, in acute PD models using 6-hydroxy dopamine (6-OHDA) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, mGluR1 or mGluR5 antagonist administration protected against dopaminergic neuronal loss in the substantia nigra (Aguirre et al, 2001;Vernon et al, 2007).…”

Anticonvulsant Effect of (RS)-1-Aminoindan-1,5-dicarboxylic Acid on Pentetrazol-Induced Kindled Seizures in Mice

“…For example, activation of group I mGluR resulted in the inhibition of GABA receptor functions and release of GABA. 5,6) Karr and Rutecki 7) reported that a group I mGluR agonist, (RS)-3,5-dihydroxyphenylglycine ((RS)-3,5-DHPG) caused epileptiform activity in rat hippocampal slices, and this model is an in vitro model of ictogenesis. In contrast, a group I mGluR antagonist had anticonvulsive effects on a number of epilepsy models, such as pilocarpine-induced status epileptics, absence seizures and sound-induced seizures 8,9) ; however, the study dealing with the participation of GABAergic system on anticonvulsive effect of group I mGluR antagonist is scanty.…”