Temporal analysis of the upregulation of GluR5 mRNA editing with age: regional evaluation

Paschen, Wulf; Schmitt, Justina; Dux, E.; Djuričić, Bogdan

doi:10.1016/0165-3806(95)00042-c

Cited by 25 publications

(14 citation statements)

References 20 publications

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“…The more extensive editing of GluK2 in dorsal horn neurons paralleled the higher expression of mRNA encoding ADAR1 and ADAR2 in dorsal horn compared to DRG. On the other hand, the overall relatively low level of mRNA editing of the other GluK subunits is consistent with the levels of editing activity previously reported for GluK1 and GluK2 transcripts in embryonic tissues from various brain regions (Paschen et al, 1995; Belcher and Howe, 1997; Bernard et al, 1999; Lee et al, 2001). Furthermore, the relatively minimal editing at the Q/R site in GluK1 and GluK2 transcripts expressed by E17 DRG neurons is consistent with the previously demonstrated expression of Ca 2+ permeable KA receptors by embryonic DRG neurons (Lee et al, 2001).…”

Section: Discussionsupporting

confidence: 91%

“…Kainate receptors containing GluK1 (formerly GluR5) or GluK2 (formerly GluR6) subunits can be Ca 2+ -permeable when the subunits are unedited (Egebjerg and Heinemann, 1993; Kohler et al, 1993). These unedited subunits are highly expressed in most brain areas during embryonic development (Paschen et al, 1994; Paschen et al, 1995). Similarly, embryonic and early postnatal nociceptive DRG neurons express unedited GluK1 and the corresponding Ca 2+ permeable KA receptors (Lee et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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Modulation of neurite outgrowth by activation of calcium‐permeable kainate receptors expressed by rat nociceptive‐like dorsal root ganglion neurons

Joseph

Williams

MacDermott

2011

Developmental Neurobiology

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Neurite outgrowth is a fundamental step in establishing proper neuronal connections in the developing central nervous system. Dynamic control of outgrowth has been attributed to changes in growth cone Ca2+ levels in response to extracellular cues. Here we have investigated a possible role for Ca2+ permeable kainate (KA) receptors in regulating neurite outgrowth of nociceptive-like dorsal root ganglion (DRG) neurons. To identify KA receptor subunits likely to be involved, we used quantitative RT-PCR on acutely dissociated DRG and dorsal horn neurons. DRG neurons expressed more GluK1, particularly the GluK1b spice variant, than dorsal horn neurons. Conversely, dorsal horn neurons expressed more GluK2, particularly GluK2a, than DRG neurons. Further, an RNA editing assay indicated that the majority of GluK1 and GluK2 mRNA transcripts in DRG were unedited. Imaging Ca2+ transients following application of a KA receptor agonist to DRG and dorsal horn co-cultures revealed increases in intracellular Ca2+ in the growth cones of DRG neurons. In the majority of cases, this increase in Ca2+ was partly or completely blocked by Joro spider toxin (JSTX), an antagonist for Ca2+-permeable AMPA and KA receptors. Treatment of DRG/dorsal horn co-cultures with KA for 18 hours suppressed neurite outgrowth while application of the rapidly desensitizing KA receptor agonist SYM 2081, the competitive AMPA/KA receptor antagonist, CNQX, and JSTX or philanthotoxin enhanced neurite outgrowth and prevented KA effects on neurite outgrowth. Thus, Ca2+ entry through KA receptors at the growth cone of DRG neurons may be an important regulator of neurite outgrowth.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Modulation of neurite outgrowth by activation of calcium‐permeable kainate receptors expressed by rat nociceptive‐like dorsal root ganglion neurons

Joseph

Williams

MacDermott

2011

Developmental Neurobiology

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“…Con A (300 g/ml for 3 min) did not completely eliminate desensitization. P4 -P25, with the degree of editing increasing to 80% in the adult (Paschen et al, 1995), we analyzed the extent of GluR5 editing during the course of postnatal development (P3, P14, and P56). In the TG, both the edited and unedited forms of the GluR5 subunit were detected at all ages (Fig.…”

Section: Current-voltage Relationmentioning

confidence: 99%

Glutamate Receptor Subunits GluR5 and KA-2 Are Coexpressed in Rat Trigeminal Ganglion Neurons

Sahara¹,

et al. 1997

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To determine the subunit composition of high-affinity kainate receptors in native neurons is a challenging problem because of the expression of more than one GluR subunit. In the present study the question of whether GluR5 and/or GluR6 subunits combine with KA-1 or KA-2 subunits in vivo is addressed by performing detailed physiological, pharmacological, and molecular characterization of functional kainate receptor channels in acutely dissociated trigeminal ganglion (TG) neurons. The results show that (1) smaller diameter TG neurons (Ͻ30 m) respond to L-glutamate and kainate, and the currents gated by kainate desensitize with prolonged agonist exposure; (2) all kainate receptor subunits are detected to some extent by reverse transcriptase-PCR, whereas glutamate receptor subunits GluR5 and KA-2 are expressed at high levels in the TG; (3) there is an obvious similarity between the features of native kainate receptor channels in TG neurons and of heteromeric recombinant GluR5(R)/KA-2 channels in pharmacological properties, desensitization, rectification, ion permeability, and mean channel conductance; and (4) the age-dependent increase in GluR5 and KA-2 RNA levels in the TG is correlated well with an increased number of kainate-sensitive cells during postnatal development. Our data suggest that the heteromeric GluR5/ KA2 combination actually occurs in TG neurons and give a clue as to the subunit composition of native kainate receptor channels.

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“…Expression of GRIK1 is developmentally regulated, with a transient peak of expression during early postnatal development at a stage of intense synaptogenesis [Bettler and Mulle, 1995]. Further diversity of GluR5 channels is generated by alternative splicing and by pre-mRNA editing [Bernard and Khrestchatisky, 1994;Paschen et al, 1995;Seeburg, 1996]. Recently, early-onset epilepsy and postnatal lethality has been demonstrated in heterozygous transgenic mice that permanently express an editingdeficient allele at the Q/R site of the glutamate receptor GluR-B gene [Brusa et al, 1995].…”

Section: Introductionmentioning

confidence: 99%

“…Recently, early-onset epilepsy and postnatal lethality has been demonstrated in heterozygous transgenic mice that permanently express an editingdeficient allele at the Q/R site of the glutamate receptor GluR-B gene [Brusa et al, 1995]. The Q/R site in GluR5, which is located in the putative ion channel forming the second transmembrane domain, is subject to developmentally controlled pre-mRNA-editing [Bernard and Khrestchatisky, 1994;Paschen et al, 1995;Seeburg, 1996]. The extent of pre-mRNA editing may influence seizure liability due to alterations of Ca 2+ permeability of the glutamate-gated channel.…”

Section: Introductionmentioning

confidence: 99%

Allelic association of juvenile absence epilepsy with a GluR5 kainate receptor gene (GRIK1) polymorphism

Sander¹,

Hildmann

Kretz³

et al. 1997

Am. J. Med. Genet.

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Juvenile absence epilepsy (JAE) is a common subtype of idiopathic generalized epilepsy (IGE). Hereditary factors play a major role in its etiology. The important function of glutamate receptors (GluRs) in excitatory neurotransmission, synaptic plasticity, and neurodevelopment suggests their involvement in epileptogenesis. A tetranucleotide repeat polymorphism in the non-coding region of the kainate-selective GluR5 receptor gene (GRIK1) on chromosome 21q22.1 provides the tool to investigate this candidate gene. The present association and linkage study tested the hypothesis that allelic variants of GRIK1 confer genetic susceptibility to the pathogenesis of JAE. Our family-based association analysis using the haplotype-based haplotype relative risk statistic revealed an association of JAE with the nine-repeat containing allele of the GRIK1 tetranucleotide polymorphism (chi2 = 8.31, df = 1, P = 0.004). Supportive evidence for linkage to a JAE related IGE spectrum (Zmax = 1.67 at GRIK1) under an autosomal dominant mode of inheritance and significant allele sharing (P < 0.05) among the affected family members suggest that allelic variants of GRIK1 contribute a major genetic determinant to the pathogenesis of JAE-related phenotypes.

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Temporal analysis of the upregulation of GluR5 mRNA editing with age: regional evaluation

Cited by 25 publications

References 20 publications

Modulation of neurite outgrowth by activation of calcium‐permeable kainate receptors expressed by rat nociceptive‐like dorsal root ganglion neurons

Modulation of neurite outgrowth by activation of calcium‐permeable kainate receptors expressed by rat nociceptive‐like dorsal root ganglion neurons

Glutamate Receptor Subunits GluR5 and KA-2 Are Coexpressed in Rat Trigeminal Ganglion Neurons

Allelic association of juvenile absence epilepsy with a GluR5 kainate receptor gene (GRIK1) polymorphism

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