Kainate receptor

They were first identified as a distinct receptor type through their selective activation by the agonist kainate, a drug first isolated from the algae Digenea simplex.

[2] Each KAR subunit begins with a 400-residue extracellular N-terminal domain, which plays a key role in assembly, followed by the first segment of the neurotransmitter-binding cleft, called S1.

M2 turns into M3, another transmembrane segment which emerges on the extracellular face to complete the neurotransmitter binding site (a portion called S2).

Differences in the ligand binding pocket allow for the development of moderately subunit-selective kainate receptor agonists and antagonists.

Recent investigation through voltage clamping has shown that kainate receptors have more than just an ionotropic (or directly changing a membrane's conductivity) role in neurons.

[6] The specific link of this pathway remains to be found, as well as the explanation for why the polarization and distribution of KARs varies so much across neurons and brain regions.

KAR expression and distribution has shown a linkage to schizophrenia, depression, autism, Huntington's, bipolar disorder, and epilepsy among others.

[8] Kainate receptors have a subtle role in synaptic plasticity, affecting the likelihood that the postsynaptic cell will fire in response to future stimulation.