Cloning of a putative glutamate receptor: A low affinity kainate-binding subunit

Bettler, Bernhard; Egebjerg, Jan; Sharma, Geeta; Pecht, Gerlinde; Hermans‐Borgmeyer, Irm; Moll, Carlo; Stevens, Charles F.; Heinemann, Stephen F.

doi:10.1016/0896-6273(92)90292-l

Cited by 365 publications

(195 citation statements)

References 55 publications

Supporting

Mentioning

179

Contrasting

Unclassified

Order By: Relevance

“…The relative proportion of these two sites in some brain areas changes during development, although as in the adult, the qualitative distribution pattern of the two sites is more or less identical . At first sight, these two sites are reflected in the recombinant kainate receptor subunits: homomeric KA-subunits have KD -5-10 nM (Werner et al, 1991;Herb et al, 1992) while homomeric configurations of GluR-5, -6, and -7 average -50-100 nM K, for kainate (Bettler et al, 1992;Lomeli et al, 1992;Sommer et al, 1992). However, since homomeric cloned KA subunits do not form functional ion channels, but assuming that they do so in vivo as partners with the GluR subunits, it is difficult to know how to precisely relate the binding to the recombinant data.…”

Section: Discussionmentioning

confidence: 99%

“…In the adult thalamus, only the reticular area has an appreciable number of binding sites and GluR-7 predominates in this nucleus (Monaghan and Cotman, 1982;Unnerstall and Wamsley, 1983;Miller et al, 1990;Bettler et al, 1992;Lomeli et al, 1992;Wisden and Seeburg, 1993;and Figs. 1, 10).…”

Section: Kainate Receptor Expression In the Developing Thalamusmentioning

confidence: 99%

“…These developmental effects are mediated directly and indirectly by the same classes ofreceptors that are used for excitatory communication and the generation of plasticity in the adult brain, namely, AMPA/low-affinity kainate (AMPA-preferring), high-affinity kainate (kainate-preferring), NMDA-gated channels and metabotropic receptors (reviewed by Young and Fagg, 1990;Monaghan and Anderson, 1991;Gasic and Hollmann, 1992;Nakanishi, 1992;Monaghan, 1993;Wisden and Seeburg 1993a,b). Kainate-preferring receptors can be constructed from subunits GluR-5, GluR-6, GluR-7, KA-1, and KA-2/y2 (Bettler et al, 1990(Bettler et al, , 1992Egebjerg et al, 1991;Werner et al, 1991;Herb et al, 1992;Lomeli et al, 1992;Sakimura et al, 1992;Sommer et al, 1992;Partin et al, 1993;Wenthold et al, 1993;reviewed Wisden and Seeburg, 1993a,b). They can be generated in vitro from recombinant homomeric (GluR-5 and GluR-6) or heteromeric configurations (e.g., KA-2/GluR-6), and form channels with rapidly desensitizing responses to kainate (Herb et al, 1992;Sakimura et al, 1992;Sommer et al, 1992), and can further be distinguished from AMPA receptors because their desensitization rate can be modulated by ConA but not cyclothiozide (Partin et al, 1993).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Kainate receptor gene expression in the developing rat brain

1994

View full text Add to dashboard Cite

Kainate-preferring receptors are a subclass of ionotropic glutamate receptors that might play a role in brain development. The expression of the five known genes encoding kainate receptor subunits (GluR-5, -6, -7, KA-1, and KA-2) was studied by in situ hybridization during pre- and postnatal development of the rat brain. We compared the combined expression patterns of these genes with autoradiography using 3H- kainate in the developing brain from embryonic day 12 (E12) through to adult. Although mRNAs for the receptor subunits (except KA-1) can be detected at stage E12, 3H-kainic acid binding (as an index of receptor protein) is not found at this stage. However, by E14 high-affinity kainate sites are found throughout the gray matter, but particularly in spinal cord, primordial cerebellum, and ventral forebrain structures. All genes undergo a peak in their expression in the late embryonic/early postnatal period. GluR-5 expression during development shows the most interesting features because the changes are qualitative. The GluR-5 gene shows peaks of expression around the period of birth in the sensory cortex (layers II, III, and IV), in CA1 hippocampal interneurons in the stratum oriens, in the septum, and in the thalamus. GluR-6 shows a prenatal expression peak in the cingulate gyrus of the neocortex. KA-1 transcripts appear with the development of the hippocampus and remain largely confined to discrete areas such as the CA3 region, the dentate gyrus, and subiculum. KA-2 transcripts are found throughout the CNS from as early as E12 and remain constant until adulthood. The GluR-5 and GluR-6 genes are coexpressed in multiple peripheral ganglia (e.g., cranial nerve ganglia, dorsal root ganglia, and mural ganglia) at E14.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Kainate Receptor Expression In the Developing Thalamusmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Kainate receptor gene expression in the developing rat brain

1994

View full text Add to dashboard Cite

show abstract

“…For GluR6, the mRNA is abundant in the dentate gyrus and also in the CA3 subregion (Egebjerg et al, 1991;Wisden and Seeburg, 1993b;Bahn et al, 1994). GluR7 is not expressed in high levels in the hippocampus, but dentate gyrus granule cells show moderate levels of mRNA for GluR7 (Bettler et al, 1992;Lomeli et al, 1992;Wisden and Seeburg, 1993b;Bahn et al, 1994). GluR5 is expressed in low levels in CA1 subregion and is almost absent in other subregions of the hippocampus (Bettler et al, 1990;Wisden and Seeburg, 1993b;Bahn et al, 1994).…”

Section: Distribution Of Mrna For Kainate Receptor Subunits In the Hmentioning

confidence: 99%

Kainate receptors in hippocampal CA3 subregion: evidence for a role in regulating neurotransmitter release

Malva

Carvalho

1998

Neurochemistry International

View full text Add to dashboard Cite

The hippocampal CA3 subregion of the rat is characteristically enriched in kainate receptors. At the synaptic level, the subcellular localization of these receptors is still a matter of debate. The CA3 pyramidal cells are particularly sensitive to excitotoxicity induced by kainate, which is in agreement with the high levels of kainate receptors in the stratum lucidum of the hippocampal CA3 subregion. Immunocytochemical studies, using antibodies against kainate receptor subunits, clearly demonstrated the presence of postsynaptic kainate receptors. However, it was not possible at the time to identify the activity of postsynaptic kainate receptors as mediators of the synaptic transmission. There are also reports showing the labeling of unmyelinated axons and nerve terminals with antibodies against kainate receptor subunits. The evidence for the presence of presynaptic kainate receptors in the hippocampus is further substantiated by the demonstration that stimulation of kainate receptors in synaptosomes isolated from the rat hippocampal CA3 subregion increases the intracellular free Ca 2÷ concentration ([Ca2+]~) coupled to the release of glutamate. These results support the model proposed by Coyle (1983), in which the excitotoxicity induced by kainate involves the activation of presynaptic kainate receptors, causing the release of glutamate. According to this model, the neurotoxic effect of kainate in the rat hippocampal CA3 subregion involves a direct effect on presynaptic kainate receptors and an indirect effect on postsynaptic glutamate receptors due to the enhanced release of glutamate.

show abstract

“…4), but only weakly activates AMPA receptors to produce steady-state currents with a very small desensitizing component. Within the kainate receptor subunit family, KA1 and KA2 kainate receptor subunits have a higher binding affinity for kainate (K D values of 5-15 nM) than do GluR5, GluR6, and GluR7 (K D values of 13-95 nM) (Bettler et al 1990(Bettler et al , 1992Werner et al 1991;Herb et al 1992;Lomeli et al 1992;Swanson et al 1997). As mentioned previously, KA1 and KA2 have been referred to as "high-affinity" kainate receptor subunits and GluR5-7 as "low-affinity" subunits; it is important to keep in mind that this nomenclature, while useful for categorizing the two sub-families of subunits, is not relevant to their sensitivities to the endogenous neurotransmitter, glutamate.…”

Section: Biological Activities Of Kainoidsmentioning

confidence: 99%

Developmental Biology of Neoplastic Growth

Macieira‐Coelho¹

2005

Progress in Molecular and Subcellular Biology

View full text Add to dashboard Cite

Cloning of a putative glutamate receptor: A low affinity kainate-binding subunit

Cited by 365 publications

References 55 publications

Kainate receptor gene expression in the developing rat brain

Kainate receptor gene expression in the developing rat brain

Kainate receptors in hippocampal CA3 subregion: evidence for a role in regulating neurotransmitter release

Developmental Biology of Neoplastic Growth

Contact Info

Product

Resources

About