Genetic ablation of the GluK4 kainate receptor subunit causes anxiolytic and antidepressant-like behavior in mice.

There is a clear link between dysregulation of glutamatergic signaling and mood disorders. Genetic variants in the glutamate receptor gene GRIK4, which encodes the kainate receptor subunit GluK4, alter the susceptibility for depression, bipolar disorder and schizophrenia. Here we demonstrate that Grik4(-/-) mice have reduced anxiety and an antidepressant-like phenotype.

High-affinity kainate receptor subunits are necessary for ionotropic but not metabotropic signaling.

Kainate receptors signal through both ionotropic and metabotropic pathways. The high-affinity subunits, GluK4 and GluK5, are unique among the five receptor subunits, as they do not form homomeric receptors but modify the properties of heteromeric assemblies. Disruption of the Grik4 gene locus resulted in a significant reduction in synaptic kainate receptor currents.

Na+/H+ antiporter, V-H+-ATPase and Na+/K+-ATPase immunolocalization in a marine teleost (Myoxocephalus octodecemspinosus).

Long-term pH compensation in a marine teleost requires the transepithelial excretion of H(+) across the gill epithelium. H(+) efflux in the longhorn sculpin (Myoxocephalus octodecemspinosus) is dependent on external sodium ion concentration and is inhibited by known inhibitors of Na(+)/H(+) exchangers. Our model for proton transport suggests acid-excreting cells in the gill with an apical Na(+)/H(+) antiporter and basolateral Na(+)/K(+)-ATPase.