The regulation of kainate receptor action

Glutamate receptor

However, the observed decline in the current magnitude of a response desensitization at recombinant kainate receptors using rapid perfusion of GluR transfected cells has been investigated. The convulsant kainic acid induces seizures, in part, by activation of kainate receptors containing the GluK2 subunit and also probably via AMPA receptors [5] Activation of kainate receptors containing the GluK1 subunit can also induce seizures but deletion of this subunit does not reduce seizure susceptibility to kainate or in other seizure models.

Several biophysical features have also been ascribed to kainate receptor-mediated responses. Intracellular polyamines are thought to confer the inward rectification to the I — V curves for unedited versions of these channels [38].

In contrast, homomeric GluR5 Q receptor currents are relatively slowly desensitizing, with an estimated t1 of 15 ms and a t2 of ms [19, 24]. A recent study has also established that 5-iodowillardine does not evoke currents from GluR7 kainate receptors [59].

Furthermore, CNS inflammation, apoptosis, and axonal damage were reduced. As we learn more of the molecular biological and biophysical properties of these ligand-gated ion channels and the regional distribution of their proteins, a realization evolves of the their potential functional roles.

Similar results were obtained with animal studies that Kainate receptor pharmacology and physiology demonstrated that formalin-induced behaviours [75] but not acute physiological nociceptive responses [89] are reduced by the GluR5-selective antagonist, LY A mouse GluR6 splice variant GluR has also been reported [25].

Discussion Together, these data show that synaptically released glutamate inhibits IsAHP acting via the metabotropic property of kainate receptors on CA1 pyramidal cells. These compelling data have set the stage for a predictably explosive increase in work on all aspects of function and hold the promise of catalyzing timely breakthroughs in therapeutic strategies.

However, somewhat conflicting results of the presynaptic inhibitory effect of kainate receptors at GABA terminals have been reported.

Agonist-induced PKC phosphorylation regulates GluK2 SUMOylation and kainate receptor endocytosis

The pharmacological properties of the agonist 2S,4R 4-methylglutamate [60] have been studied in a variety of neuronal and nonneuronal preparations. Glucocorticoid action in cells is mediated by a specific receptor protein, the glucocorticoid receptor GR.

For recombinant homomeric receptors comprised of GluR6 Q unedited subunits, agonist responses result in channels with appreciable calcium permeability and inwardly rectifying current-voltage relationships [24, 40, 35].

M4 begins extracellularly, and passes again through the membrane into the cytoplasm, forming the C-terminal of the protein. M2 turns into M3, another transmembrane segment which emerges on the extracellular face to complete the neurotransmitter binding site a portion called S2.

Metabotropic Regulation of Intrinsic Excitability by Synaptic Activation of Kainate Receptors

Intracellular modulation of kainate receptors Biochemical studies have examined the phosphorylation of GluR6 receptors and correlated this with enhancement of ion channel function by protein kinase A PKA [50].

This segment, termed the "p loop," determines the calcium permeability of the receptor. Prolonged changes in neuronal excitability can result from modulation of intrinsic conductances.

Glutamate Receptor Ion Channels: Structure, Regulation, and Function

This article has been cited by other articles in PMC.Kainic acid is an excitoxic glutamate analog that is well known to increase neuronal excitability and generate seizurelike activity. The conventional view of th. The action of lectins appears to be via binding to the carbohydrate side chain of the kainate receptor protein [81].

Also revealed was that although N-glycosylation of the receptor was not required for glutamate receptor function per se, it was essential for modulation of channel activity by lectins.

Kerchner GA, Wilding TJ, Huettner JE, Zhuo M: Kainate receptor subunits underlying presynaptic regulation of transmitter release in the dorsal horn.

J Neurosci– PubMed Google Scholar. Here we ascribe a new physiological function to this metabotropic kainate receptor (mKAR) in which glutamate released from excitatory afferents in area CA1 of the hippocampus mimics the action of kainate on these receptors. The surface expression and regulated endocytosis of kainate (KA) receptors (KARs) plays a critical role in neuronal function.

PKC can modulate KAR trafficking, but the sites of action and molecular consequences have not been fully characterized.

Small ubiquitin-like modifier (SUMO) modification of the KAR subunit GluK2 mediates agonist-evoked. Metabotropic signaling by kainate receptors. Ricardo J. Rodrigues and; Juan Lerma * Article first published online: 11 JAN Lancaster B.

Metabotropic-mediated kainate receptor regulation of IsAHP and excitability in pyramidal cells. Protein kinase signalling requirements for metabotropic action of kainate receptors in rat CA1.

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The regulation of kainate receptor action
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