Expression of glutamate receptor genes in white matter: developing and adult rat optic nerve

Am, Jensen; Sy, Chiu

doi:10.1523/jneurosci.13-04-01664.1993

Cited by 59 publications

(43 citation statements)

References 41 publications

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“…Other studies have focused on the NMDA, AMPA, and kainic acid subtypes in development [Insel et al, 1990;Monyer et al, 1991;Pellegrini-Giampietro et al, 1991Sato et al, 1993;Durand and Zukin, 1993;Jensen and Chiu, 1993;Standley et al, 1993;Bahn et al, 1994;Monyer et al, 1994;Riva et al, 1994;Sheng et al, 1994;Jakowec et al, 1995a, b] and in the adult [Monaghan et al, 1984;Petralia and Wenthold, 1992;Wenthold et al, 1992;Martin et al, 1993a, b]. Our study confirms the observations of others, as well as further contributes by focusing on changes of the AMPA receptor subunit transcripts and their proteins in the basal ganglia in ontogenesis.…”

Section: Discussionsupporting

confidence: 90%

The Postnatal Development of AMPA Receptor Subunits in the Basal Ganglia of the Rat

Jakowec

Jackson‐Lewis²,

et al. 1998

Dev Neurosci

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In situ hybridization and immunohistochemistry were used to characterize the expression pattern of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors during postnatal development in the rat basal ganglia. All subunit transcripts showed some degree of developmental regulation. GluR1 and GluR2 are expressed at high levels in the neonate with reduced expression in the adult. GluR3 and GluR4 are expressed at significantly lower levels in both neonates and adults and have much more modest degrees of reduced expression in adults as compared with GluR1 and GluR2. Analysis of the flip and flop transcript isoforms indicates that GluR1 flip and flop and GluR2 flip are the predominately expressed splice variants in adults. Observed changes in the expression of the AMPA receptor transcripts indicate that there are fundamental differences in the expression of these receptor subunits in adults and neonates. This phenomenon may play a significant role in the establishment of proper synaptic circuitry within the developing basal ganglia in early postnatal life as well as contributing to differences in susceptibility to injury and disease in the aging brain.

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Section: Discussionsupporting

confidence: 90%

The Postnatal Development of AMPA Receptor Subunits in the Basal Ganglia of the Rat

Jakowec

Jackson‐Lewis²,

et al. 1998

Dev Neurosci

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“…Astrocytes have traditionally been viewed to have a role in the metabolic and trophic support of neurons (Jensen and Chiu, 1993). Their position at the interface of blood vessels and synapses is consistent with these roles.…”

Section: Discussionmentioning

confidence: 98%

“…Their position at the interface of blood vessels and synapses is consistent with these roles. Astrocytes and neurons interact at many levels (Chiu andKriegler, 1994), including GJIC (Charles, 1994;Nedergaard, 1994). It is clear that neurons can regulate GJIC through neurotransmitters.…”

Section: Discussionmentioning

confidence: 99%

Connexin43 null mutation increases infarct size after stroke

Siushansian

Bechberger

Cechetto

et al. 2001

J of Comparative Neurology

143

106

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Glial-neuronal interactions have been implicated in both normal information processing and neuroprotection. One pathway of cellular interactions involves gap junctional intercellular communication (GJIC). In astrocytes, gap junctions are composed primarily of the channel protein connexin43 (Cx43) and provide a substrate for formation of a functional syncytium implicated in the spatial buffering capacity of astrocytes. To study the function of gap junctions in the brain, we used heterozygous Cx43 null mice, which exhibit reduced Cx43 expression. Western blot analysis showed a reduction in the level of Cx43 protein and GJIC in astrocytes cultured from heterozygote mice. The level of Cx43 is reduced in the adult heterozygote cerebrum to 40% of that present in the wild-type. To assess the effect of reduced Cx43 and GJIC on neuroprotection, we examined brain infarct volume in wild-type and heterozygote mice after focal ischemia. In our model of focal stroke, the middle cerebral artery was occluded at two points, above and below the rhinal fissure. Four days after surgery, mice were killed, the brains were sectioned and analyzed. Cx43 heterozygous null mice exhibited a significantly larger infarct volume compared with wild-type (14.4 +/- 1.4 mm(3) vs. 7.7 +/- 0.82 mm(3), P < 0.002). These results suggest that augmentation of GJIC in astrocytes may contribute to neuroprotection after ischemic injury.

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“…Reverse transcription into cDNA was carried out using random hexamer primers and avian myeloblastosis virus reverse transcriptase (United States Biochemical) as described by the supplier. Specific oligonucleotide primers as well as PCR reagent concentrations used for PCR amplification of each AMPA and kainate receptor subunits were as described earlier (8,9). Primers (20 to 22 mers) specific for NMDA receptor subunits were designed to amplify with equal efficiency all the described splice variants of the NMDAR1 subunit (bases 600 to 1134, clone accession no.…”

Section: Methodsmentioning

confidence: 99%

Glutamate receptor-mediated toxicity in optic nerve oligodendrocytes

Matute

Sánchez‐Gómez

Martínez‐Millán

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

328

267

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In cultured oligodendrocytes isolated from perinatal rat optic nerves, we have analyzed the expression of ionotropic glutamate receptor subunits as well as the effect of the activation of these receptors on oligodendrocyte viability. Reverse transcription-PCR, in combination with immunocytochemistry, demonstrated that most oligodendrocytes differentiated in vitro express the ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunits GluR3 and GluR4 and the kainate receptor subunits GluR6, GluR7, KA1 and KA2. Acute and chronic exposure to kainate caused extensive oligodendrocyte death in culture. This effect was partially prevented by the AMPA receptor antagonist GYKI 52466 and was completely abolished by the non-N-methyl-Daspartate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), suggesting that both AMPA and kainate receptors mediate the observed kainate toxicity. Furthermore, chronic application of kainate to optic nerves in vivo resulted in massive oligodendrocyte death which, as in vitro, could be prevented by coinfusion of the toxin with CNQX. These findings suggest that excessive activation of the ionotropic glutamate receptors expressed by oligodendrocytes may act as a negative regulator of the size of this cell population.The main function of oligodendrocytes is to myelinate axons in the vertebrate central nervous system. This cell type develops mostly soon after the majority of neurons are generated and have extended their axons and, therefore, it is likely that neurons play an important role in regulating oligodendrocyte development. In the rat optic nerve, the first fully differentiated oligodendrocytes appear after birth, and the definitive mature population of oligodendrocytes is reached around 6 weeks later (1, 2). The proliferation and the survival of oligodendrocytes depend, respectively, on the electrical activity of neighboring axons and in the reciprocal contacts they establish (for a recent review, see ref.3). Axon to oligodendrocyte signaling results in the generation of the precise number of oligodendrocytes necessary to myelinate entirely a given population of axons. Unfortunately, little information is available about the molecules participating in this signaling process.Oligodendrocytes express neurotransmitter receptors including those activated by glutamate (4). This excitatory amino acid acts at various types of receptors, which can be grouped into two major categories: ionotropic receptors, which gate membrane ion channels permeable to cations; and metabotropic receptors, which are coupled to G proteins. Ionotropic receptors are classified into ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate, and N-methyl-Daspartate (NMDA) subtypes, according to their preferred agonist. Molecular cloning has revealed that each receptor subtype is composed of several subunits with high homology within each receptor class (reviewed in ref. 5). Thus, AMPA receptors are formed by GluR1-4, kainate receptors by GluR5-7 and KA1-2, and NMDA rece...

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Expression of glutamate receptor genes in white matter: developing and adult rat optic nerve

Cited by 59 publications

References 41 publications

The Postnatal Development of AMPA Receptor Subunits in the Basal Ganglia of the Rat

The Postnatal Development of AMPA Receptor Subunits in the Basal Ganglia of the Rat

Connexin43 null mutation increases infarct size after stroke

Glutamate receptor-mediated toxicity in optic nerve oligodendrocytes

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