2-Substituted (2SR)-2-Amino-2-((1SR,2SR)-2-carboxycycloprop-1-yl)glycines as Potent and Selective Antagonists of Group II Metabotropic Glutamate Receptors. 1. Effects of Alkyl, Arylalkyl, and Diarylalkyl Substitution

1998 ◽  
Vol 41 (3) ◽  
pp. 346-357 ◽  
Author(s):  
Paul L. Ornstein ◽  
Thomas J. Bleisch ◽  
M. Brian Arnold ◽  
Rebecca A. Wright ◽  
Bryan G. Johnson ◽  
...  
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate ◽  
Selective Antagonists ◽  
Group Ii

scholarly journals HDAC and HAT Inhibitors Differently Affect Analgesia Mediated by Group II Metabotropic Glutamate Receptors

2014 ◽  
Vol 10 ◽  
pp. 1744-8069-10-68 ◽  
Author(s):  
Magda Zammataro ◽  
Maria Angela Sortino ◽  
Carmela Parenti ◽  
Robert W Gereau ◽  
Santina Chiechio
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate ◽  
Group Ii

Potentiation of Morphine's Antinociception by Group II and Group III Metabotropic Glutamate Receptors Agonists on a Rat Incisional Pain

2006 ◽  
Vol 19 (2) ◽  
pp. 131 ◽  
Author(s):  
Chang Mo Kim ◽  
Jeong Il Choi ◽  
Hong Beom Bae ◽  
Seok Jai Kim ◽  
Sung Tae Chung ◽  
...  
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Group Iii ◽  
Metabotropic Glutamate ◽  
Group Ii ◽  
Incisional Pain

The striatum as a target for anti-rigor effects of an antagonist of mGluR1, but not an agonist of group II metabotropic glutamate receptors

2002 ◽  
Vol 950 (1-2) ◽  
pp. 88-94 ◽  
Author(s):  
Krystyna Ossowska ◽  
Jolanta Konieczny ◽  
Andrzej Pilc ◽  
Stanisław Wolfarth
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate ◽  
Group Ii

scholarly journals Metabotropic glutamate receptors and glutamate transporters shape transmission at the developing retinogeniculate synapse

2013 ◽  
Vol 109 (1) ◽  
pp. 113-123 ◽  
Author(s):  
Jessica L. Hauser ◽  
Eleanore B. Edson ◽  
Bryan M. Hooks ◽  
Chinfei Chen
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Time Course ◽  
Ganglion Cells ◽  
Glutamate Transporters ◽  
Decay Kinetics ◽  
Metabotropic Glutamate ◽  
Glutamate Concentration ◽  
Group Ii ◽  
Retinogeniculate Synapse

Over the first few postnatal weeks, extensive remodeling occurs at the developing murine retinogeniculate synapse, the connection between retinal ganglion cells (RGCs) and the visual thalamus. Although numerous studies have described the role of activity in the refinement of this connection, little is known about the mechanisms that regulate glutamate concentration at and around the synapse over development. Here we show that interactions between glutamate transporters and metabotropic glutamate receptors (mGluRs) dynamically control the peak and time course of the excitatory postsynaptic current (EPSC) at the immature synapse. Inhibiting glutamate transporters by bath application of TBOA (dl- threo-β-benzyloxyaspartic acid) prolonged the decay kinetics of both α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) and N-methyl-d-aspartate receptor (NMDAR) currents at all ages. Moreover, at the immature synapse, TBOA-induced increases in glutamate concentration led to the activation of group II/III mGluRs and a subsequent reduction in neurotransmitter release at RGC terminals. Inhibition of this negative-feedback mechanism resulted in a small but significant increase in peak NMDAR EPSCs during basal stimulation and a substantial increase in the peak with coapplication of TBOA. Activation of mGluRs also shaped the synaptic response during high-frequency trains of stimulation that mimic spontaneous RGC activity. At the mature synapse, however, the group II mGluRs and the group III mGluR7-mediated response are downregulated. Our results suggest that transporters reduce spillover of glutamate, shielding NMDARs and mGluRs from the neurotransmitter. Furthermore, mechanisms of glutamate clearance and release interact dynamically to control the glutamate transient at the developing retinogeniculate synapse.

scholarly journals Activation of group II metabotropic glutamate receptors blocks zinc release from hippocampal mossy fibers

2014 ◽  
Vol 47 (1) ◽  
pp. 73 ◽  
Author(s):  
Carlos M Matias ◽  
Jose C Dionísio ◽  
Peter Saggau ◽  
Maria Quinta-Ferreira
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Mossy Fibers ◽  
Metabotropic Glutamate ◽  
Zinc Release ◽  
Group Ii

Selective Inhibition of Spontaneous But Not Ca2+-Dependent Release Machinery by Presynaptic Group II mGluRs in Rat Cerebellar Slices

2006 ◽  
Vol 96 (1) ◽  
pp. 86-96 ◽  
Author(s):  
Maike Glitsch
Keyword(s):  
Action Potential ◽  
Glutamate Receptors ◽  
Neurotransmitter Release ◽  
Metabotropic Glutamate Receptors ◽  
Gaba Release ◽  
Spontaneous Release ◽  
Metabotropic Receptors ◽  
Voltage Gated ◽  
Metabotropic Glutamate ◽  
Group Ii

Two main forms of neurotransmitter release are known: action potential-evoked and spontaneous release. Action potential-evoked release depends on Ca2+entry through voltage-gated Ca2+channels, whereas spontaneous release is thought to be Ca2+-independent. Generally, spontaneous and action potential-evoked release are believed to use the same release machinery to release neurotransmitter. This study shows, using the whole cell patch-clamp technique in rat cerebellar slices, that at the interneuron- Purkinje cell synapse activation of presynaptic group II metabotropic glutamate receptors suppresses spontaneous GABA release through a mechanism independent of voltage-gated Ca2+channels, store-operated Ca2+channels, and Ca2+release from intracellular Ca2+stores, suggesting that the metabotropic receptors target the release machinery directly. Voltage gated Ca2+channel-independent release following increased presynaptic cAMP production is similarly inhibited by these metabotropic receptors. In contrast, both voltage-gated Ca2+channel-dependent and presynaptic N-methyl-d-aspartate receptor-dependent GABA release were unaffected by activation of group II metabotropic glutamate receptors. Hence, the mechanisms underlying spontaneous and Ca2+-dependent GABA release are distinct in that only the former is blocked by group II metabotropic glutamate receptors. Thus the same neurotransmitter, glutamate, can activate or inhibit neurotransmitter release by selecting different receptors that target different release machineries.

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