An object of the present invention is to provide a null mutant non-human animal
showing salt intake behavior similar to that of wild-type animals under water-sufficient
conditions and showing much more intakes of hypertonic saline compared with wild-type
animals under water- and salt-depleted conditions, for example, an Nav2
gene-deficient non-human animal, which is useful as a model animal of excessive
salt intake experiments.
The object will be attained by following process: mouse genomic libraries are
screened with rat NaG cDNA as a probe, then Nav2 gene of genomic DNA
is isolated, and a targeting vector is constructed by inserting marker gene such
as neo gene into the exon of Nav2. After thus constructed targeting
vector is induced to ES cells, homologously recombined ES cells are selected, then
germ line chimeric mice are constructed with this ES cells strain, and they are
hybridized with the wild-type mice and heterozygous mutant mice are obtained. By
intercrossing of thus obtained heterozygous mutant mice, Nav2 knockout
mice are constructed.