|1.||Gasparini, Fabrizio: 11 articles (09/2015 - 07/2002)|
|2.||Conn, P Jeffrey: 11 articles (10/2014 - 07/2003)|
|3.||Faden, Alan I: 10 articles (06/2015 - 01/2006)|
|4.||Gomez-Mancilla, Baltazar: 9 articles (09/2015 - 05/2010)|
|5.||Danysz, Wojciech: 9 articles (12/2011 - 04/2006)|
|6.||Brownell, Anna-Liisa: 7 articles (11/2015 - 09/2007)|
|7.||Ametamey, Simon M: 7 articles (05/2015 - 02/2007)|
|8.||Neugebauer, Volker: 7 articles (02/2014 - 01/2004)|
|9.||Folsom, Timothy D: 6 articles (09/2015 - 01/2011)|
|10.||Fatemi, S Hossein: 6 articles (09/2015 - 01/2011)|
02/01/2014 - "To restore mPFC activity and hence control pain-related amygdala hyperactivity this study focused on CB1 and mGluR5 receptors, which are important modulators of cortical functions. "
12/01/2007 - "The present study aimed at determining whether persistent inflammatory pain produces alterations in intracellular and plasma membrane-associated mGluR1alpha and mGluR5 in spinal cord dorsal horn. "
11/04/2015 - "The regulation of the VPS26A-SNX27 interaction that modifies mGluR5 trafficking and expression in the dorsal horn provides a novel therapeutic strategy for pain relief."
11/15/2014 - "Recently we reported on a bivalent ligand (MMG22) containing both mu agonist and mGluR5 antagonist pharmacophores that produced potent antinociception in mice with LPS-induced acute inflammatory pain via a putative MOR-mGluR5 heteromer. "
02/01/2014 - "The data suggest that excited mPFC neurons are inversely linked to amygdala output (CeLC) and that CB1 can increase mGluR5 function in this subset of mPFC neurons to engage cortical control of abnormally enhanced amygdala output in pain. "
|2.||Schizophrenia (Dementia Praecox)
07/01/2015 - "Environmental Enrichment Ameliorates Behavioral Impairments Modeling Schizophrenia in Mice Lacking Metabotropic Glutamate Receptor 5."
07/01/2015 - "The results from our study provide compelling evidence that mGluR5 regulation is altered in schizophrenia, likely contributing to the altered glutamatergic signaling that is associated with the disorder."
07/01/2015 - "Human genetic and pharmacological animal studies support this hypothesis, but no studies have explored mGluR5 dysfunction at the molecular level in the postmortem schizophrenia brain. "
01/01/2014 - "The majority of studies in the schizophrenia post-mortem brain indicate that total mGluR5 expression is unaltered. "
05/01/2013 - "Despite its potential, molecular studies characterising mGluR5 in schizophrenia are limited. "
|3.||Autistic Disorder (Autism)
03/01/2010 - "Our findings suggest that antagonists of mGluR5 receptors may have selective therapeutic efficacy in treating repetitive behaviors in autism."
04/25/2012 - "We used BTBR T+tf/J (BTBR) mice, an established model with robust behavioral phenotypes relevant to the three diagnostic behavioral symptoms of autism--unusual social interactions, impaired communication, and repetitive behaviors--to probe the efficacy of a selective negative allosteric modulator of the mGluR5 receptor, GRN-529. "
10/01/2015 - "Decreased expression of mGluR5 within the dorsolateral prefrontal cortex in autism and increased microglial number in mGluR5 knockout mice: Pathophysiological and neurobehavioral implications."
03/01/2015 - "The failure of the metabotropic glutamate receptor 5 antagonists falls on the heels of the failure of Arbaclofen's efficacy in children and adults with autism or FXS. "
06/01/2014 - "Long-term memory deficits are associated with elevated synaptic ERK1/2 activation and reversed by mGluR5 antagonism in an animal model of autism."
07/01/2009 - "These data demonstrate that mGluR5 activation can reduce microglial-associated inflammation, suggesting that the protective effects of mGluR5 agonists may reflect this action. "
12/30/2005 - "These results provide direct functional evidence that blockade of peripheral mGluR5 receptors inhibits nociceptive transmission and support previous studies demonstrating a peripheral site of action associated with the antinociceptive effect of MPEP following inflammation."
06/01/2015 - "The selective mGluR5 agonist CHPG attenuates SO2-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells."
01/01/2015 - "The end point immunohistochemical analyses verified the enhanced mGluR5 expression and inflammation. "
01/01/2015 - "Using PET imaging, we showed that pharmacological activation of mGluR5 during 5 weeks reduced expression of classic inflammation marker PBR in many brain areas and that this molecular association was not present in LPS-exposed offspring. "
|5.||Brain Injuries (Brain Injury)
04/01/2012 - "Thus, potentiating mGluR5 activity with selective agonists such as CHPG may be useful for the treatment of traumatic brain injury."
06/01/2015 - "In present study, we aimed to evaluate whether activation of mGluR5 attenuates early brain injury (EBI) after experimental SAH in rats. "
01/01/2014 - "Recent studies show that neurodegeneration and neuroinflammation after traumatic brain injury can be inhibited as late as one month in animals by the activation of the metabotropic glutamate receptor 5 in microglia using (RS)-2-chloro-5- hydroxy-phenylglycine. "
10/01/2014 - "Novel mGluR5 positive allosteric modulator improves functional recovery, attenuates neurodegeneration, and alters microglial polarization after experimental traumatic brain injury."
01/18/2013 - "Activation of metabotropic glutamate receptor 5 reduces the secondary brain injury after traumatic brain injury in rats."
|1.||metabotropic glutamate receptor type 1
|2.||Metabotropic Glutamate Receptors (Metabotropic Glutamate Receptor)
|3.||Glutamic Acid (Glutamate)
|4.||Levodopa (L Dopa)
|5.||metabotropic glutamate receptor 2
|6.||Cocaine (Cocaine HCl)
|8.||metabotropic glutamate receptor 3 (mGluR3)
|9.||Proteins (Proteins, Gene)
|10.||Ethanol (Ethyl Alcohol)
|1.||Self Administration (Administration, Self)
|3.||Drug Therapy (Chemotherapy)