Evidence that the metabotropic glutamate receptor 5 antagonist MPEP may act as an inhibitor of the norepinephrine transporter in vitro and in vivo

Synapse ◽  
2003 ◽  
Vol 50 (4) ◽  
pp. 269-276 ◽  
Author(s):  
Christian A. Heidbreder ◽  
Massimiliano Bianchi ◽  
Laurent P. Lacroix ◽  
Stefania Faedo ◽  
Elisabetta Perdona ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Norepinephrine Transporter ◽  
Metabotropic Glutamate Receptor 5 ◽  
Metabotropic Glutamate

scholarly journals Metabotropic glutamate receptor signaling is required for NMDA receptor-dependent ocular dominance plasticity and LTD in visual cortex

2015 ◽  
Vol 112 (41) ◽  
pp. 12852-12857 ◽  
Author(s):  
Michael S. Sidorov ◽  
Eitan S. Kaplan ◽  
Emily K. Osterweil ◽  
Lothar Lindemann ◽  
Mark F. Bear
Keyword(s):  
Visual Cortex ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Excitatory Synapses ◽  
Ocular Dominance Plasticity ◽  
Metabotropic Glutamate

A feature of early postnatal neocortical development is a transient peak in signaling via metabotropic glutamate receptor 5 (mGluR5). In visual cortex, this change coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD). However, loss of visual responsiveness after MD occurs via mechanisms revealed by the study of long-term depression (LTD) of synaptic transmission, which in layer 4 is induced by acute activation of NMDA receptors (NMDARs) rather than mGluR5. Here we report that chronic postnatal down-regulation of mGluR5 signaling produces coordinated impairments in both NMDAR-dependent LTD in vitro and ocular dominance plasticity in vivo. The data suggest that ongoing mGluR5 signaling during a critical period of postnatal development establishes the biochemical conditions that are permissive for activity-dependent sculpting of excitatory synapses via the mechanism of NMDAR-dependent LTD.

scholarly journals Metabotropic glutamate receptor 3 activation is required for long-term depression in medial prefrontal cortex and fear extinction

2015 ◽  
Vol 112 (4) ◽  
pp. 1196-1201 ◽  
Author(s):  
Adam G. Walker ◽  
Cody J. Wenthur ◽  
Zixiu Xiang ◽  
Jerri M. Rook ◽  
Kyle A. Emmitte ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Fear Extinction ◽  
Long Term Depression ◽  
Metabotropic Glutamate ◽  
Metabotropic Glutamate Receptor 3

Clinical studies have revealed that genetic variations in metabotropic glutamate receptor 3 (mGlu3) affect performance on cognitive tasks dependent upon the prefrontal cortex (PFC) and may be linked to psychiatric conditions such as schizophrenia, bipolar disorder, and addiction. We have performed a series of studies aimed at understanding how mGlu3 influences PFC function and cognitive behaviors. In the present study, we found that activation of mGlu3 can induce long-term depression in the mouse medial PFC (mPFC) in vitro. Furthermore, in vivo administration of a selective mGlu3 negative allosteric modulator impaired learning in the mPFC-dependent fear extinction task. The results of these studies implicate mGlu3 as a major regulator of PFC function and cognition. Additionally, potentiators of mGlu3 may be useful in alleviating prefrontal impairments associated with several CNS disorders.

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