Molecular Diversity of Glutamate Receptors and Implications for Brain Function

Nakanishi, Shigetada

doi:10.1126/science.1329206

Cited by 2,460 publications

(1,460 citation statements)

References 67 publications

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“…Animal studies on the binding of ketamine suggest lower affinity in the cerebellum than in the hippocampus (Yoneda and Ogita 1991) and the forebrain (Porter and Greenamyre 1995). The cerebellum is rich in the NMDAR2C subunit whereas the NMDAR2A and NMDAR2B subunits are expressed more strongly in the cortex and hippocampus (Nakanishi 1992). Also, in a recent study of subjects with cerebellar degeneration, Moschner et al (1999) found a significant increase in latency and decreased acceleration of eye movement initiation whereas we found only decreases in acceleration.…”

Section: Discussionsupporting

confidence: 40%

Ketamine Effects on Eye Movements

Weiler

Thaker

Lahti

et al. 2000

Neuropsychopharmacology

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Section: Discussionsupporting

confidence: 40%

Ketamine Effects on Eye Movements

Weiler

Thaker

Lahti

et al. 2000

Neuropsychopharmacology

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“…CaSR displays significant homology with metabotropic glutamate receptors (mGluRs) expressed in the brain (Nakanishi, 1992;Ruat et al, 1995), and it has been shown that some types of mGluRs, including mGluR3 and mGluR5, are activated not only by glutamate but also by extracellular Ca 2 + (Kubo et al, 1998), although the physiological relevance of this Ca 2 + -sensing property remains unknown. Interesting, similarly to CaSR, in a previous work we found an increased expression of mGluR3 and mGluR5 one week after ibotenic acid or kainate-induced lesions in the rat brain.…”

Section: Discussionmentioning

confidence: 99%

Identification of calcium sensing receptor (CaSR) mRNA-expressing cells in normal and injured rat brain

et al. 2009

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Calcium sensing receptor (CaSR), isolated for the first time from bovine and human parathyroid, is a G-protein-coupled receptors that has been involved in diverse physiological functions. At present a complete in vivo work on the identification of CaSR mRNA-expressing cells in the adult brain lacks and this investigation was undertaken in order to acquire more information on cell type expressing CaSR mRNA in the rat brain and to analyse for the first time its expression in different experimental models of brain injury.The expression of CaSR mRNAs was found mainly in scattered cells throughout almost all the brain regions. A double labeling analysis showed a colocalization of CaSR mRNA expression in neurons and oligodendrocytes, whereas it was not found expressed both in the microglia and in astrocytes. One week after kainate-induced seizure CaSR was found in the injured CA3 region of the hippocampus and very interestingly it was found upregulated in the neurons of CA1-CA2 and dentate gyrus. Similarly, 1 week following ibotenic acid injection in the hippocampus, CaSR mRNA expression was increased in oligodendrocytes both in the lesioned area and in the contralateral CA1-CA3 pyramidal cell layers and dentate gyrus. One week after needle-induced mechanical lesion an increase of labeled cells expressing CaSR mRNA was observed along the needle track. In conclusion, the present results contribute to extend available data on cell type-expressing CaSR in normal and injured brain and could spur to understand the role of CaSR in repairing processes of brain injury.

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“…The aldehydeconjugated drug could potentially interact with the antibodies, since the D-APV binding site (Nakanishi, 1992;Mori and Mishina, 1995) resides near the antigenic site (Sheng et al, 1994). However, there are several reasons why we think this interpretation is unlikely.…”

Section: D-apv Causes Trafficking Of Nr2b Subunits Away From Synapsesmentioning

confidence: 94%

In vivo blockade of N-methyl-d-aspartate receptors induces rapid trafficking of NR2B subunits away from synapses and out of spines and terminals in adult cortex

Fujisawa

Aoki

2003

Neuroscience

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We investigated the role of in vivo synaptic activity upon trafficking of the N-methyl-D-aspartate (NMDA) receptor subunit, NR2B, at mature synapses by electron microscopic immunocytochemistry. In vivo blockade of NMDA receptors was achieved by applying the NMDA receptor antagonist, D-2-amino-5-phosphonovalerate (D-APV), onto the cortical surface of one hemisphere of anesthetized adult rats. Inactive L-2-amino-5-phosphonovalerate (L-APV) was applied to the contralateral hemisphere for within-animal control and to assess basal level of NR2B subunits at synapses. Within 30 min of D-APV treatment, we observed a decrease in the number of layer I axospinous asymmetric synapses that are positively immuno-labeled for the NR2B subunits. This decrease was paralleled by reductions in the absolute number of immuno-gold particles found at these synapses. The decrease of NR2B labeling was detectable in all five animals examined. Significant reductions were seen not only at post-synaptic densities, but also within the cytoplasm of spines and axon terminals. The data demonstrate that blockade of NMDA receptors induces trafficking of NR2B subunits out of synaptic membranes, spines, and terminals. This is in sharp contrast to a previous observation that NR2A subunits move into spines and axon terminals following in vivo blockade with D-APV. These findings point to yet unknown, NMDA receptor activitydependent mechanisms that separately regulate the localization of NR2A and NR2B subunits at synapses. Keywordsactivity-dependent; D-APV; electron microscopy; immunocytochemistry; ultrastructure; postembedding colloidal gold labelingThe N-methyl-D-aspartate (NMDA) subtype of glutamate receptor plays an important role in experience-dependent plasticity. Calcium influx through this receptor can trigger a variety of downstream biochemical reactions, contributing to plasticity (Mori and Mishina, 1995;Kind and Neumann, 2001) and excitotoxicity (Lynch and Guttmann, 2002). One of many consequences of NMDA receptor activation is altered trafficking of proteins to and from the activated synapses. For example, long-term potentiation, in which the electrophysiological response to an input is augmented, is in part produced by NMDA receptor-dependent upregulation of synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (see NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2010 May 24. Malenka and Nicoll, 1999). In vitro and fewer in vivo preparations have been used to demonstrate that NMDA receptors, too, are removed from or inserted into synaptic membrane (Rao and Craig, 1997;Liao et al., 1999;Quinlan et al., 1999;Heynen et al., 2000;Barria and Malinow, 2002;Grosshans et al., 2002;Tovar and Westbrook, 2002). However, since nearly all of these studies have used neonatal tissues, whether or not such dynamic properties of NMDA receptor subunits persist at mature synapses, in vivo, is a topic that remains relatively unexplored.Among the NMDA receptor subunits, the NR1 is necessary for NMD...

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Molecular Diversity of Glutamate Receptors and Implications for Brain Function

Cited by 2,460 publications

References 67 publications

Ketamine Effects on Eye Movements

Ketamine Effects on Eye Movements

Identification of calcium sensing receptor (CaSR) mRNA-expressing cells in normal and injured rat brain

In vivo blockade of N-methyl-d-aspartate receptors induces rapid trafficking of NR2B subunits away from synapses and out of spines and terminals in adult cortex

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