Regular ArticleMetabotropic Glutamate Receptors and Cell-Type-Specific Vulnerability in the Striatum: Implication for Ischemia and Huntington's Disease
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Glutamate receptor endocytosis and signaling in neurological conditions
2023, Progress in Molecular Biology and Translational ScienceImShot: An Open-Source Software for Probabilistic Identification of Proteins In Situ and Visualization of Proteomics Data
2022, Molecular and Cellular ProteomicsSelective basal ganglia vulnerability to energy deprivation: Experimental and clinical evidences
2018, Progress in NeurobiologyMetabotropic glutamate receptors and neurodegenerative diseases
2017, Pharmacological ResearchCitation Excerpt :Inhibition of presynaptic glutamate release through activation of Group II and III mGluRs has been proposed as a potential strategy to limit excitotoxicity. In the striatum, Group II and III mGluRs are mainly located on corticostriatal presynaptic terminals, mediating a negative feedback control for glutamate release [218,245,246]. Importantly, R6/2 HD transgenic mice treated with the mGluR2/3 agonist LY379268 (1.2 mg/kg VO) exhibited increased survival time (about 10% increase) and diminished early pathological hyperactivity, although rotarod deficit and htt intranuclear inclusions were not ameliorated by LY379268 treatment [213].
Metabotropic glutamate receptor 5 upregulates surface NMDA receptor expression in striatal neurons via CaMKII
2015, Brain ResearchCitation Excerpt :This CaMKII-dependent mGluR5-NMDAR coupling is in accordance with the observations that (1) DHPG activated CaMKII in striatal and hippocampal neurons (Choe and Wang, 2001; Mockett et al., 2011; Jin et al., 2013b; this study), (2) Ca2+ or DHPG readily recruited active CaMKII to GluN2B (Leonard et al., 1999; Colbran, 2004; Bayer et al., 2006; Jin et al., 2013b), and (3) mGluR5 signals enhanced phosphorylation of GluN2B at S1303 (Jin et al., 2013b; this study), a CaMKII-sensitive site where phosphorylation augmented NMDAR currents (Liao et al., 2001). Of note, protein kinase C (PKC), an effector downstream to the mGluR5-diacylglycerol pathway, also phosphorylates NMDAR subunits at multiple sites including S1303 (Omkumar et al., 1996; Tingley et al., 1997; Liao et al., 2001) and contributes to the mGluR5 potentiation of NMDAR activity (Pisani et al., 1997; Calabresi et al., 1999). It is therefore likely that CaMKII and PKC act in concert to connect mGluR5 to NMDARs to control synaptic transmission.
The mGluR5 positive allosteric modulator, CDPPB, ameliorates pathology and phenotypic signs of a mouse model of Huntington's disease
2015, Neurobiology of DiseaseCitation Excerpt :Neuropathological analysis reveals selective and progressive neuronal loss in the striatum (DiFiglia, 1990; Vonsattel et al., 1985). Glutamate-mediated neurotoxicity has been postulated to play an important role in the pathogenesis of HD (Anborgh et al., 2005; Calabresi et al., 1999; DiFiglia, 1990; Ribeiro et al., 2010). Stimulation of metabotropic glutamate receptor 5 (mGluR5) leads to the formation of inositol 1,4,5-trisphosphate (InsP3) and release of intracellular Ca2 + and mutant htt can enhance this cell signaling pathway, leading to toxic levels of intracellular Ca2 + (Ribeiro et al., 2010; Tang et al., 2005; Tang et al., 2003).