Kir4.1f/f floxed mice possess loxP sites flanking the entire open reading frame of the potassium inwardly-rectifying channel, subfamily J, member 10 (Kcnj10) gene. Inward-rectifying Kir4.1 channels are mediators of astrocyte potassium buffering during neuronal activity. Mice that are homozygous for this allele are viable and fertile. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have the Kir4.1 gene deleted in the cre-expressing tissues.
When bred to mice expressing Cre recombinase in astrocytes via the human glial fibrillary acidic protein promoter, offspring die prematurely and display severe ataxia and stress-induced seizures. They exhibit severe depolarization of both passive astrocytes and complex glia and impairment of both potassium and glutamate uptake. Membrane and action potential properties of CA1 pyramidal neurons, as well as basal synaptic transmission in the CA1 stratum radiatum, are unaffected, whereas spontaneous neuronal activity is reduced.
