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Grin2d  -  glutamate receptor, ionotropic, NMDA2D...

Mus musculus

Synonyms: GluN2D, GluRepsilon4, Glutamate receptor ionotropic, NMDA 2D, N-methyl D-aspartate receptor subtype 2D, NMDAR2D, ...
 
 
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Disease relevance of Grin2d

 

Psychiatry related information on Grin2d

  • GluRepsilon4 mutant mice showed reduced spontaneous locomotor activity in a novel environment and less sensitivity to stress induced by the elevated plus-maze, light-dark box, and forced swimming tests [3].
 

High impact information on Grin2d

  • In mature mice, overexpression of NR2D was associated with a reduction of both NR2B and Ca2+-independent activity of Ca2+- and calmodulin-dependent protein kinase II [4].
  • The effects of changing NMDA receptor subunit composition on synaptic plasticity in the hippocampus were analyzed by creating transgenic mice overexpressing NR2D, a predominantly embryonic NMDA receptor subunit [4].
  • RT-PCR studies revealed that GluRepsilon1 and GluRepsilon4 subunit mRNAs were transcribed by both non-induced and neuronally differentiated cells [5].
  • The NR2D subunit is normally present at very low levels in the mature forebrain [1].
  • By immunofluorescence microscopy using the specific subunit antibodies and fluorescence-labeled secondary antibodies, the distinctly expressed NR1a and NR2D subunits could be located in the plasma membrane of the transformed yeast cells [6].
 

Biological context of Grin2d

  • Our experiments suggest that although both diheteromeric and triheteromeric NR2D-containing receptors are expressed in cerebellar Golgi cells, neither receptor type participates in parallel fiber to Golgi cell synaptic transmission [7].
  • The genes encoding the ionotropic N-methyl-D-aspartate (NMDA) receptor subunits NR1a, NR2B and NR2D were cloned in the multi-copy yeast-Escherichia coli shuttle vectors pMBO1 and pMB02 [6].
 

Anatomical context of Grin2d

 

Associations of Grin2d with chemical compounds

  • These findings suggest that GluRepsilon4 mutant mice have dysfunctional NMDA receptors and altered emotional behavior probably caused by changes in monoaminergic neuronal activities in adulthood [3].
  • GluRepsilon4 mutant mice exhibited reductions of [(3)H]MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate] binding and (45)Ca(2+) uptake through the NMDA receptors [3].
  • While wild-type, GluRepsilon1(-/-), GluRepsilon4(-/-), and GluRepsilon1(-/-)/epsilon4(-/-) mice all died by ammonium chloride at 12 mmol/kg during the first tonic convulsions, two of eight GluRepsilon3(-/-) mice survived [8].
 

Regulatory relationships of Grin2d

 

Other interactions of Grin2d

  • Until P21, however, all of these subunits were down-regulated with particular reduction for GluRepsilon2 and GluRepsilon4 mRNAs [9].
  • However, we could find no difference in the properties of NMDAR-mediated EPSCs between wild-type and NR2D subunit ablated mice [7].
  • PPDC was identified as a new class of NMDA-receptor antagonist because it has a mode of action different from that of the previous antagonists; it selectivly binds the GluRepsilon3/GluRzeta1 and GluRepsilon4/GluRzeta1 subtype receptors in an agonist-independent allosteric manner [10].

References

  1. Suppression of epileptogenesis by modification of N-methyl-D-aspartate receptor subunit composition. Bengzon, J., Okabe, S., Lindvall, O., McKay, R.D. Eur. J. Neurosci. (1999) [Pubmed]
  2. Characterization of N-methyl-D-aspartate receptor subunits responsible for postoperative pain. Nishimura, W., Muratani, T., Tatsumi, S., Sakimura, K., Mishina, M., Minami, T., Ito, S. Eur. J. Pharmacol. (2004) [Pubmed]
  3. Lower sensitivity to stress and altered monoaminergic neuronal function in mice lacking the NMDA receptor epsilon 4 subunit. Miyamoto, Y., Yamada, K., Noda, Y., Mori, H., Mishina, M., Nabeshima, T. J. Neurosci. (2002) [Pubmed]
  4. Hippocampal synaptic plasticity in mice overexpressing an embryonic subunit of the NMDA receptor. Okabe, S., Collin, C., Auerbach, J.M., Meiri, N., Bengzon, J., Kennedy, M.B., Segal, M., McKay, R.D. J. Neurosci. (1998) [Pubmed]
  5. Schedule of NMDA receptor subunit expression and functional channel formation in the course of in vitro-induced neurogenesis. Varju, P., Schlett, K., Eisel, U., Madarász, E. J. Neurochem. (2001) [Pubmed]
  6. Molecular and pharmacological characterization of recombinant rat/mice N-methyl-D-aspartate receptor subtypes in the yeast Saccharomyces cerevisiae. Becker, J., Li, Z., Noe, C.R. Eur. J. Biochem. (1998) [Pubmed]
  7. NR2B and NR2D subunits coassemble in cerebellar Golgi cells to form a distinct NMDA receptor subtype restricted to extrasynaptic sites. Brickley, S.G., Misra, C., Mok, M.H., Mishina, M., Cull-Candy, S.G. J. Neurosci. (2003) [Pubmed]
  8. Characterization of N-methyl-D-aspartate receptor subunits involved in acute ammonia toxicity. Kitano, T., Matsumura, S., Seki, T., Hikida, T., Sakimura, K., Nagano, T., Mishina, M., Nakanishi, S., Ito, S. Neurochem. Int. (2004) [Pubmed]
  9. Early onset of NMDA receptor GluR epsilon 1 (NR2A) expression and its abundant postsynaptic localization in developing motoneurons of the mouse hypoglossal nucleus. Oshima, S., Fukaya, M., Masabumi, N., Shirakawa, T., Oguchi, H., Watanabe, M. Neurosci. Res. (2002) [Pubmed]
  10. (1S,2R)-1-Phenyl-2-[(S)-1-aminopropyl]-N,N-diethylcyclopropanecarboxamide (PPDC), a new class of NMDA-receptor antagonist: molecular design by a novel conformational restriction strategy. Shuto, S., Yoshii, K., Matsuda, A. Jpn. J. Pharmacol. (2001) [Pubmed]
 
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