GluK2 is a subunit of the kainate receptor family of glutamate-gated ion channels. The human subunit is encoded by GRIK2; the older name GluR6 occurs in much of the originating experimental literature. A receptor subunit is a component of an assembled channel, not a synonym for every member of the kainate receptor family.[ref]
https://www.ncbi.nlm.nih.gov/mesh/2106638. NLM GluK2 Kainate Receptor entry, including historical GluR6 names
Deleting the gene for the subunit gave a direct test of its functional contribution. C. Mulle and colleagues generated GluR6-deficient mice and found reduced sensitivity to kainic acid in hippocampal CA3 neurons. A postsynaptic kainate current evoked by trains of mossy-fibre stimulation was absent in the mutants. The mice were also less susceptible to the tested systemic-kainate seizure challenge.[ref]
Altered synaptic physiology and reduced susceptibility to kainate-induced seizures in GluR6-deficient mice by C. Mulle and others. Nature 392,601–605(1998), abstract: gene disruption, CA3 response, train-evoked current and challenge endpoints.
For an experimental comparison, disappearance of a stimulus-evoked current after deleting GluK2 supports a requirement for that subunit in the tested response. It does not establish that every excitatory current in the same cell is a GluK2 current: AMPA receptors and other receptors can still contribute different components. Nor does gene deletion, by itself, specify the subunit composition of every remaining channel. Combining molecular perturbation with a precisely defined stimulation protocol makes the inference much stronger than interpreting an agonist response alone.
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