Kainate Receptors

Kainate receptors are cation-selective, ligand-gated ion channels, which cause a strong membrane depolarization in response to glutamate binding. Like other members of the ionotropic glutamate receptor family, they are named for their specific activation by kainate (kainic acid), which was initially isolated from the algae Digenea simplex.

Kainate receptors exist as tetramers, composed of the subunits GluK1 to 5. Each subunit has an extracellular N-terminus, a cytoplasmic C-terminus, three membrane-spanning segments and a re-entrant loop that dips into the membrane from the cytoplasmic face to form the pore. It is thought that subunits GluK4 and K5 (formerly named KA1 and KA2, respectively) act as modulatory subunits, conferring high affinity binding for glutamate. When expressed in vitro, homomeric receptors of GluK1 or K2 subunits are non-functional.

The GluK1 and K2 subunits of kainate receptors, like the GluA2 subunit found in AMPA receptors may undergo post-translation modification at a specific amino acid residue within the re-entrant loop, termed the Q/R site. The amino acid expressed at this site, either glutamine (Q) or arginine (R), modulates the Ca²⁺ permeability of the ion channel.

Kainate receptors are expressed on the presynaptic membrane of both excitatory and inhibitory synapses, where their actions either facilitate or inhibit neurotransmitter release. Activation of kainate receptors results in increased cation permeability and depolarization of the presynaptic neuron. The subunit conformation, and therefore Ca²⁺ permeability, of a specific kainate receptor has an effect on its presynaptic modulatory activity.

Compared to other glutamate receptors, kainate receptors play a relatively small role in excitatory synaptic signaling. When expressed on postsynaptic membranes they produce small, slow excitatory postsynaptic potentials (EPSPs). These small changes in ion balance affect the overall likelihood of postsynaptic cell firing.

Kainate receptors have been linked to development of temporal lobe epilepsy in humans. Additionally, kainate dosing can be used to generate an animal model of epilepsy via a process known as kindling. It is thought that this occurs via activation of GluK4 and K5 containing receptors, which are highly expressed in the hippocampus, the likely site of seizure onset in this model. Alleles of the GluK2 subunit have also been linked to Huntington's disease, autism and schizophrenia.

External sources of pharmacological information for Kainate Receptors :

• IUPHAR Receptor Code

• BJP Guide

Literature for Kainate Receptors

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Addiction Poster

The key feature of drug addiction is the inability to stop using a drug despite clear evidence of harm. This poster describes the brain circuits associated with addiction, and provides an overview of the main classes of addictive drugs and the neurotransmitter systems that they target.

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Parkinson's Disease Poster

Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.

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Kainate Receptor Gene Data