scholarly journals Regulation of phosphorylation of NMDA receptor NR1 subunits in the rat neostriatum by group I metabotropic glutamate receptors in vivo

2006 ◽  
Vol 394 (3) ◽  
pp. 246-251 ◽  
Author(s):  
Eun Sang Choe ◽  
Eun Ha Shin ◽  
John Q. Wang
Keyword(s):  
Nmda Receptor ◽  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate ◽  
Group I

scholarly journals Functional Cross-Talk between Adenosine and Metabotropic Glutamate Receptors

2019 ◽  
Vol 17 (5) ◽  
pp. 422-437 ◽  
Author(s):  
David Agustín León-Navarro ◽  
José Luis Albasanz ◽  
Mairena Martín
Keyword(s):  
Neurodegenerative Diseases ◽  
Adenylyl Cyclase ◽  
Glutamate Receptors ◽  
G Protein ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Gene And Protein Expression

G-protein coupled receptors are transmembrane proteins widely expressed in cells and their transduction pathways are mediated by controlling second messenger levels through different G-protein interactions. Many of these receptors have been described as involved in the physiopathology of neurodegenerative diseases and even considered as potential targets for the design of novel therapeutic strategies. Endogenous and synthetic allosteric and orthosteric selective ligands are able to modulate GPCRs at both gene and protein expression levels and can also modify their physiological function. GPCRs that coexist in the same cells can homo- and heteromerize, therefore, modulating their function. Adenosine receptors are GPCRs which stimulate or inhibit adenylyl cyclase activity through Gi/Gs protein and are involved in the control of neurotransmitter release as glutamate. In turn, metabotropic glutamate receptors are also GPCRs which inhibit adenylyl cyclase or stimulate phospholipase C activities through Gi or Gq proteins, respectively. In recent years, evidence of crosstalk mechanisms between different GPCRs have been described. The aim of the present review was to summarize the described mechanisms of interaction and crosstalking between adenosine and metabotropic glutamate receptors, mainly of group I, in both in vitro and in vivo systems, and their possible use for the design of novel ligands for the treatment of neurodegenerative diseases.

scholarly journals Phosphorylation of group I metabotropic glutamate receptors (mGluR1/5) in vitro and in vivo

2008 ◽  
Vol 55 (4) ◽  
pp. 403-408 ◽  
Author(s):  
Li-Min Mao ◽  
Xian-Yu Liu ◽  
Guo-Chi Zhang ◽  
Xiang-Ping Chu ◽  
Eugene E. Fibuch ◽  
...  
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate ◽  
Group I

β-Amyloid Peptides Impair PKC-Dependent Functions of Metabotropic Glutamate Receptors in Prefrontal Cortical Neurons

2005 ◽  
Vol 93 (6) ◽  
pp. 3102-3111 ◽  
Author(s):  
Joanna P. Tyszkiewicz ◽  
Zhen Yan
Keyword(s):  
Nmda Receptor ◽  
Glutamate Receptors ◽  
Cortical Neurons ◽  
Metabotropic Glutamate Receptors ◽  
Pyramidal Neurons ◽  
Amyloid Peptide ◽  
Metabotropic Glutamate ◽  
Prefrontal Cortical ◽  
Group I ◽  
Β Amyloid

The metabotropic glutamate receptors (mGluRs) have been implicated in cognition, memory, and some neurodegenerative disorders, including the Alzheimer's disease (AD). To understand how the dysfunction of mGluRs contributes to the pathophysiology of AD, we examined the β-amyloid peptide (Aβ)-induced alterations in the physiological functions of mGluRs in prefrontal cortical pyramidal neurons. Two potential targets of mGluR signaling involved in cognition, the GABAergic system and the N-methyl-d-aspartate (NMDA) receptor, were examined. Activation of group I mGluRs with (S)-3,5-dihydroxyphenylglycine (DHPG) significantly increased the spontaneous inhibitory postsynaptic current (sIPSC) amplitude, and this effect was protein kinase C (PKC) sensitive. Treatment with Aβ abolished the DHPG-induced enhancement of sIPSC amplitude. On the other hand, activation of group II mGluRs with (2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate (APDC) significantly increased the NMDA receptor (NMDAR)-mediated currents via a PKC-dependent mechanism, and Aβ treatment also diminished the APDC-induced potentiation of NMDAR currents. In Aβ-treated slices, both DHPG and APDC failed to activate PKC. These results indicate that the mGluR regulation of GABA transmission and NMDAR currents is impaired by Aβ treatment probably due to the Aβ-mediated interference of mGluR activation of PKC. This study provides a framework within which the role of mGluRs in normal cognitive functions and AD can be better understood.

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