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Gria3  -  glutamate receptor, ionotropic, AMPA 3

Rattus norvegicus

Synonyms: AMPA-selective glutamate receptor 3, GLUR3, GluA3, GluR-3, GluR-C, ...
 
 
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Disease relevance of Gria3

  • In kainate-induced epilepsy we could reproduce the late increase (12-24 h) in GluR-3 mRNA in the dentate gyrus; however, under this experimental condition, no clear decrease of GluR-1 expression can be observed in this area [1].
  • These results indicate a possible role for changes in AMPA receptor subunit expression in NTS neurones, involving an increase in GluR3 associated with development of hypertension in SH [2].
  • NMDAR-1, GluR2 and GluR3 mRNAs were expressed in the large neurones (type I) of the ganglion which innervate inner hair cells (IHCs), a sensory cell type likely to use an excitatory amino acid as a neurotransmitter [3].
 

High impact information on Gria3

  • Cloned AMPA receptors carrying the "flop" splice variants of glutamate receptor subtype C (GluR-C) and GluR-D are shown to have desensitization time constants of around 1 millisecond, whereas those with the "flip" variants are about four times slower [4].
  • Three closely related genes, GluR1, GluR2, and GluR3, encode receptor subunits for the excitatory neurotransmitter glutamate [5].
  • GluR2 in this pool is extensively complexed with GluR3 but not with GluR1, which is mainly confined to the cell surface [6].
  • Subtle differences in these contacts provide a structural explanation for why GluR2 L483Y and GluR3 L507Y are nondesensitizing, but GluR6, which has a tyrosine at that site, is not [7].
  • GluR-3 exhibited more modest peaks in neocortex and hippocampus [8].
 

Biological context of Gria3

  • In conclusion the results reported in the present paper reveal a specific regulation of GluR gene expression in the granule cells of the hippocampal dentate gyrus and stimulate further investigation on the functional role of the GluR-3 subunit in the receptor-channel complex [1].
  • A large decline in GluR3-expressing oligodendrocytes suggests that this subunit may be associated with the induction of apoptosis in white matter glia, thus contributing to secondary injury mechanisms [9].
  • From our data, we conclude that neurons of nuclei involved in binaural processing exhibit a specific "auditory AMPA receptor" which consists primarily of GluR-C flop and -D flop and often lacks GluR-B subunits; this indicates fast kinetics and high Ca(2+) permeability of AMPA receptor currents [10].
  • Introducing a binding site for NSF into GluR3 (GluR3NSF) generates a subunit that behaves like GluR2 in terms of kinetics and site of surface insertion [11].
  • The up-regulation of GluR3 mRNA in this model may cause a molecular change that induces the selective vulnerability of motor neurons to KA by increasing the proportion of GluR2-lacking (i.e. calcium-permeable) AMPA receptors [12].
 

Anatomical context of Gria3

  • Furthermore, a subpopulation of round cells in the ventral cochlear nucleus, and fusiform cells in the dorsal cochlear nucleus, expressed the GluR3 subunit at greatly reduced levels compared to neighboring cells [13].
  • Neurons receiving synaptic input from the auditory nerve, including globular, round, spherical, and fusiform cells, expressed GluR2, GluR3, and GluR4 subunits [13].
  • In the CA1 layer of the hippocampus, a parallel decrease of both GluR-1 and GluR-3 expression is found 12-24 h after drug treatment, followed by a recovery of the expression to control values at 48 h [1].
  • Furthermore, the absence of GluR2 and/or GluR3 in both vulnerable and resistant interneurons subtypes indicates that knowledge of receptor subunit composition is not sufficient to predict neuronal vulnerability [14].
  • GluR2 and GluR3 expression in the spiral ganglion appeared well before birth, and reached adult levels several days before the onset of function in the cochlea [15].
 

Associations of Gria3 with chemical compounds

  • The coexpression of GluR-K2 with either GluR-K3 or GluR-K1 results in the formation of channels whose current-voltage relationships differ from those of the individual subunits alone and more closely approximate the properties of kainate receptors in neurons [16].
  • In this specific brain subregion an increase of GluR-3 mRNA level is induced 12 h after LiCl/pilocarpine treatment, while a clear decrease in GluR-1 mRNA level and no significant change in GluR-2 mRNA level can be observed in the same area under these experimental conditions [1].
  • In situ hybridization (ISH) using digoxigenin-labeled riboprobes showed that mRNAs coding for GluR1 and GluR3 were located in cells in all layers of the areas examined and also in the underlying white matter [17].
  • Treatment of ovariectomized juvenile rats with estradiol induced expression of GluR1 mRNA but did not alter levels of GluR2 or GluR3 mRNA [18].
  • In a non-pyramidal neuronal population that expresses AMPA receptors characterized by high Ca(2+) permeability, the numbers of GluR1, GluR3 and GluR4 mRNA molecules harvested per cell were 354 +/- 64, 25 +/- 17 and 168 +/- 36, respectively (n = 8) [19].
 

Physical interactions of Gria3

  • These results suggest that drastic alterations in the diversity of GluR2/GluR3/NR1 receptor complexes in the surviving spiral ganglion cells, which result in alterations in Ca2+ permeability, may contribute to the deafness-related alterations in the structure and function of the cochlea [20].
 

Co-localisations of Gria3

 

Regulatory relationships of Gria3

  • The number of Fos-positive GnRH neurones that coexpressed GluR3 peaked at 12.00 h in young rats but showed little change from 12.00-20.00 h in MA-PE rats [22].
  • However, GluR3 mRNA was preferentially expressed by neurons coexpressing substance P and enkephalin and GluR4 mRNA was not detected in identified medium spiny neurons [23].
 

Other interactions of Gria3

 

Analytical, diagnostic and therapeutic context of Gria3

References

  1. Changes in gene expression of AMPA-selective glutamate receptor subunits induced by status epilepticus in rat brain. Condorelli, D.F., Belluardo, N., Mudò, G., Dell'Albani, P., Jiang, X., Giuffrida-Stella, A.M. Neurochem. Int. (1994) [Pubmed]
  2. Increased expression of AMPA receptor subunits in the nucleus of the solitary tract in the spontaneously hypertensive rat. Saha, S., Spary, E.J., Maqbool, A., Asipu, A., Corbett, E.K., Batten, T.F. Brain Res. Mol. Brain Res. (2004) [Pubmed]
  3. Co-expression of NMDA and AMPA/kainate receptor mRNAs in cochlear neurones. Safieddine, S., Eybalin, M. Neuroreport (1992) [Pubmed]
  4. A molecular determinant for submillisecond desensitization in glutamate receptors. Mosbacher, J., Schoepfer, R., Monyer, H., Burnashev, N., Seeburg, P.H., Ruppersberg, J.P. Science (1994) [Pubmed]
  5. Molecular cloning and functional expression of glutamate receptor subunit genes. Boulter, J., Hollmann, M., O'Shea-Greenfield, A., Hartley, M., Deneris, E., Maron, C., Heinemann, S. Science (1990) [Pubmed]
  6. RNA editing at arg607 controls AMPA receptor exit from the endoplasmic reticulum. Greger, I.H., Khatri, L., Ziff, E.B. Neuron (2002) [Pubmed]
  7. Structure of the kainate receptor subunit GluR6 agonist-binding domain complexed with domoic acid. Nanao, M.H., Green, T., Stern-Bach, Y., Heinemann, S.F., Choe, S. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  8. Differential expression of three glutamate receptor genes in developing rat brain: an in situ hybridization study. Pellegrini-Giampietro, D.E., Bennett, M.V., Zukin, R.S. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  9. Changes in glial cell white matter AMPA receptor expression after spinal cord injury and relationship to apoptotic cell death. Park, E., Liu, Y., Fehlings, M.G. Exp. Neurol. (2003) [Pubmed]
  10. Expression of AMPA receptor subunit flip/flop splice variants in the rat auditory brainstem and inferior colliculus. Schmid, S., Guthmann, A., Ruppersberg, J.P., Herbert, H. J. Comp. Neurol. (2001) [Pubmed]
  11. NSF interaction is important for direct insertion of GluR2 at synaptic sites. Beretta, F., Sala, C., Saglietti, L., Hirling, H., Sheng, M., Passafaro, M. Mol. Cell. Neurosci. (2005) [Pubmed]
  12. Slow and selective death of spinal motor neurons in vivo by intrathecal infusion of kainic acid: implications for AMPA receptor-mediated excitotoxicity in ALS. Sun, H., Kawahara, Y., Ito, K., Kanazawa, I., Kwak, S. J. Neurochem. (2006) [Pubmed]
  13. Expression of AMPA-selective glutamate receptor subunits in morphologically defined neurons of the mammalian cochlear nucleus. Hunter, C., Petralia, R.S., Vu, T., Wenthold, R.J. J. Neurosci. (1993) [Pubmed]
  14. AMPA receptors in the rat and primate hippocampus: a possible absence of GluR2/3 subunits in most interneurons. Leranth, C., Szeidemann, Z., Hsu, M., Buzsáki, G. Neuroscience (1996) [Pubmed]
  15. Distribution of non-NMDA glutamate receptor mRNAs in the developing rat cochlea. Luo, L., Brumm, D., Ryan, A.F. J. Comp. Neurol. (1995) [Pubmed]
  16. A family of glutamate receptor genes: evidence for the formation of heteromultimeric receptors with distinct channel properties. Nakanishi, N., Shneider, N.A., Axel, R. Neuron (1990) [Pubmed]
  17. Localization of AMPA-selective glutamate receptor subunits in the adult cat visual cortex. Gutiérrez-Igarza, K., Fogarty, D.J., Pérez-Cerdá, F., Doñate-Oliver, F., Albus, K., Matute, C. Vis. Neurosci. (1996) [Pubmed]
  18. Hormonal regulation of glutamate receptor gene expression in the anteroventral periventricular nucleus of the hypothalamus. Gu, G., Varoqueaux, F., Simerly, R.B. J. Neurosci. (1999) [Pubmed]
  19. Absolute quantification of AMPA receptor subunit mRNAs in single hippocampal neurons. Tsuzuki, K., Lambolez, B., Rossier, J., Ozawa, S. J. Neurochem. (2001) [Pubmed]
  20. Deafness induced up-regulation of GluR2/3 and NR1 in the spiral ganglion cells of the rat cochlea. Hasegawa, T., Doi, K., Fuse, Y., Fujii, K., Uno, Y., Nishimura, H., Kubo, T. Neuroreport (2000) [Pubmed]
  21. The AMPA glutamate receptor GluR3 is enriched in oxytocinergic magnocellular neurons and is localized at synapses. Ginsberg, S.D., Price, D.L., Blackstone, C.D., Huganir, R.L., Martin, L.J. Neuroscience (1995) [Pubmed]
  22. Expression of AMPA receptor subunits (GluR1-GluR4) in gonadotrophin-releasing hormone neurones of young and middle-aged persistently oestrous rats during the steroid-induced luteinising hormone surge. Bailey, J.D., Centers, A., Jennes, L. J. Neuroendocrinol. (2006) [Pubmed]
  23. Physiological and molecular properties of AMPA/Kainate receptors expressed by striatal medium spiny neurons. Stefani, A., Chen, Q., Flores-Hernandez, J., Jiao, Y., Reiner, A., Surmeier, D.J. Dev. Neurosci. (1998) [Pubmed]
  24. Widespread expression of the AMPA receptor GluR2 subunit at glutamatergic synapses in the rat spinal cord and phosphorylation of GluR1 in response to noxious stimulation revealed with an antigen-unmasking method. Nagy, G.G., Al-Ayyan, M., Andrew, D., Fukaya, M., Watanabe, M., Todd, A.J. J. Neurosci. (2004) [Pubmed]
  25. Expression of glutamate receptor genes in the mammalian retina: the localization of GluR1 through GluR7 mRNAs. Hamassaki-Britto, D.E., Hermans-Borgmeyer, I., Heinemann, S., Hughes, T.E. J. Neurosci. (1993) [Pubmed]
  26. Parvalbumin-containing interneurons in rat hippocampus have an AMPA receptor profile suggestive of vulnerability to excitotoxicity. Moga, D., Hof, P.R., Vissavajjhala, P., Moran, T.M., Morrison, J.H. J. Chem. Neuroanat. (2002) [Pubmed]
  27. Neuron-to-glia signaling mediated by excitatory amino acid receptors regulates ErbB receptor function in astroglial cells of the neuroendocrine brain. Dziedzic, B., Prevot, V., Lomniczi, A., Jung, H., Cornea, A., Ojeda, S.R. J. Neurosci. (2003) [Pubmed]
  28. Molecular and immunochemical characterization of the ionotropic glutamate receptors in the rat heart. Gill, S.S., Pulido, O.M., Mueller, R.W., McGuire, P.F. Brain Res. Bull. (1998) [Pubmed]
  29. Expression of glutamate receptor genes in white matter: developing and adult rat optic nerve. Jensen, A.M., Chiu, S.Y. J. Neurosci. (1993) [Pubmed]
  30. Heterogeneity of AMPA receptors in the dorsal column nuclei of the rat. Popratiloff, A., Rustioni, A., Weinberg, R.J. Brain Res. (1997) [Pubmed]
  31. Axon-target interactions maintain synaptic gene expression in retinae transplanted to intracranial regions of the rat. Hoover, F., Hankin, M.H., Radel, J.D., Reese, J.S., Goldman, D. Brain Res. Mol. Brain Res. (1997) [Pubmed]
 
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