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This study provides information concerning the changes in the expression of GABAergic and glutamatergic markers in mice lacking the mGlu5.
We report that expr (show PAM Proteins)ession of a key regulator of synaptic protein synthesis, the metabotropic glutamate receptor 5 (mGlu5) protein, is significantly reduced in both the brains of RS model mice and in the motor cortex of human RS autopsy samples.
once at the inner nuclear membrane, mGluR5 is stably retained via interactions with chromatin and is perfectly positioned to regulate nucleoplasmic Ca(2 (show CA2 Proteins)+)in situ
Overall, these data posit mGluR5 in key paralimbic areas as a strong determinant of the temperament trait novelty seeking. These data add to our understanding of how brain neurochemistry accounts for the variation in human behavior and strongly support further research on mGluR5 as a potential therapeutic target in neuropsychiatric disorders associated with abnormal novelty-seeking behaviors.
Decrease of mGluR5 receptor density goes parallel with changes in enkephalin and substance P (show TAC1 Proteins) immunoreactivity in Huntington's disease
The metabotropic glutamate (show GRIN1 Proteins) receptor subtype 5 (mGluR5) has been implicated in the pathophysiology of mood and anxiety disorders.
The interaction between GRM5 and cellular prion protein (show PRNP Proteins) has a central role in transgenic mouse model of Alzheimer's disease pathogenesis.
Data suggest that metabotropic glutamate receptors recycling is completely dependent on the activity of PP2A whereas, PP2B has partial effect on this process.
findings provide evidence for decreased expression of metabotropic glutamate receptor 5 and its signaling components representing a key pathophysiological hallmark in autism spectrum disorder.
Study provided evidence that protein expression of mGluR5 is significantly higher (total: 42%; monomer: 25%; dimer: 52%) in the hippocampal CA1 (show CA1 Proteins) region of schizophrenia subjects relative to healthy controls
Study identified an unexpected age-linked recovery of synaptic gain function in Fragile X (show FMR1 Proteins) syndrome (FXS) model mice medial prefrontal cortex. Stimulus evoked long-term depression mediated by endocannabinoids, absent in early adulthood (2-month-old), is recovered with senescence (at 1-year-old); recovery depends on the engagement of alternative mGlu5 coupled mechanisms.
Study shows that blocking of metabotropic glutamate (show GRIN1 Proteins) type 5 receptor (mGlu5) reduced the dysregulation of glutamate (show GRIN1 Proteins) transmission and improved motor coordination in the Grm1crv4 mouse model of cerebellar ataxia SCAR13 (show GRM1 Proteins).
The authors here demonstrate that metabotropic glutamate (show GRIN1 Proteins) receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing sleep-wake homeostasis.
mGluR5 was significantly more mobile at synapses in hippocampal Fmr1 (show FMR1 Proteins) KO neurons, causing an increased synaptic surface co-clustering of mGluR5 and NMDAR (show GRIN1 Proteins).
Results support positive allosteric modulation of mGlu5, particularly with VU0409551, as a viable mechanism to reverse the deficits in NMDA receptor function, synaptic plasticity, and memory that are known to be impaired in schizophrenia.
Collectively, these results indicate that selective antagonism of glutamate (show GRIN1 Proteins) and mGluR5 has a potentially beneficial effect in both liver cancer and Parkinson's disease, and thus may provide more understanding for the clinical investigation and further an additional therapeutic target for these two diseases.
beta-arrestin2 (show ARRB2 Proteins)-biased negative modulators of mGlu5 offer significant advantages over first-generation inhibitors for the treatment of fragile X (show FMR1 Proteins) and related disorders.
mGluR5 and CB1 (show CNR1 Proteins) act in concert to activate neuroprotective cell signaling pathways and promote neuronal survival.
This study confirmed the presence of mGluR1 (show GRM1 Proteins)/5 complex by (i) reverse immunoprecipitation using an mGluR1 (show GRM1 Proteins) antibody to pulldown mGluR5 from hippocampal tissue.
Here, we show in a mouse model of Rett syndrome (Mecp2 KO) that metabotropic glutamate receptor 5 (mGluR5)- and protein-synthesis-dependent synaptic plasticity are abnormal in the hippocampus.
L-glutamate is the major excitatory neurotransmitter in the central nervous system and activates both ionotropic and metabotropic glutamate receptors. Glutamatergic neurotransmission is involved in most aspects of normal brain function and can be perturbed in many neuropathologic conditions. The metabotropic glutamate receptors are a family of G protein-coupled receptors, that have been divided into 3 groups on the basis of sequence homology, putative signal transduction mechanisms, and pharmacologic properties. Group I includes GRM1 and GRM5 and these receptors have been shown to activate phospholipase C. Group II includes GRM2 and GRM3 while Group III includes GRM4, GRM6, GRM7 and GRM8. Group II and III receptors are linked to the inhibition of the cyclic AMP cascade but differ in their agonist selectivities. Multiple transcript variants encoding different isoforms have been found for this gene.
metabotropic glutamate receptor 5
, metabotropic glutamate receptor 5 variant F
, metabotropic glutamate receptor 5 variant G
, metabotropic glutamate receptor 5 variant H
, metabotropic glutamate receptor (mGluR5)
, metabotropic glutamate receptor 5b
, G protein coupled receptor, family C, group 1, member E
, G protein-coupled receptor GRM5
, G protein-coupled receptor, family C, group 1, member E
, metabotropic glutamate receptor subtype 5b
, metabotropic glutamate receptor type 5