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References in periodicals archive ?
Hampson, "Palmitoylation of the GluR6 kainate receptor," Proceedings of the National Academy of Sciences of the United State of America, vol.
This current study focused on the gene expression of two iGluRs: GluN1, which encodes the NMDA receptor subunit 1, and GluK1, which encodes the kainate receptor subunit 1.
Our previous study showed that there is glutamatergic tonic inhibition on GABAergic neurotransmission through the non-NMDA receptor, GluR5-containing kainate receptor.[sup][14] In the present study, DNQX, a non-NMDA glutamatergic antagonist, significantly induced the increase of sIPSCs in the control and etomidate exposure groups, which suggests that there is glutamatergic tonic inhibition on GABAergic neurotransmission; etomidate exposure did not affect the glutamatergic tonic inhibition on GABAergic neurotransmission.
Further studies of GluK2 function in brain and drug effects on this kainate receptor under normal and pathological conditions are urgently needed.
The competitive AMPA/ kainate receptor antagonist LY293558 (tezampanel) reversed and prevented LID in parkinsonian rats [40] and the non-competitive AMPA/kainate antagonist LY300164 (talampanel) decreased LID in MPTP-treated monkeys by up to 40% [41].
This fine balance between phosphorylation and SUMOylation is dependent on brain activity levels where damaging activity that occurs during stroke or epilepsy will enhance SUMOylation and therefore reduce kainate receptor function to protect nerve cells.
There are three families of glutamate-gated ion channels, named for the compounds that were used to initially identify these channels: (1) the A-methyl-D-aspartate (NMDA) receptor, (2) the [alpha]-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) receptor, and (3) the kainate receptor (AMPA and kainate receptors are collectively known as non-NMDA receptors).
Soman induces ictogenesis in the amygdala and interictal activity in the hippocampus that are blocked by a GluR5 kainate receptor antagonist in vitro.
In addition, parallel processes that are not directly related to NMDA receptors, like presynaptic forms of LTP induced by kainate receptor or AC/PKA activation and LTD that is dependent on metabotropic glutamate receptors, are present early in development and dissipate as neural circuits mature.
In particular, the invention provides a method of inducing a permanent change in the neurological development of a rodent, such as a rat, comprising daily administration of low doses of a kainate receptor agonist to the animal in the second postnatal week, wherein after treatment with the kainate receptor agonist the animal exhibits reproducible seizure-like symptoms when exposed to mild to moderate stressors.
Excitotoxicity appears to be primarily dependent on NMDA and kainate receptor activation.
The timing of this study is very opportune since three independent groups have recently isolated the kainate receptor protein as well as the gene, thus the receptor itself will soon be available for study.