| 16504 | Q63959 | KCNC3_MOUSE | Potassium voltage-gated channel subfamily C member 3 (KSHIIID) (Voltage-gated potassium channel subunit Kv3.3) | DISRUPTION PHENOTYPE | Mice lacking both Kcnc3 and Kcnc1 are born at the expected Mendelian rate, but the pups do not thrive and all die about 26 days after birth when kept together with other littermates. Their failure to thrive may be due to motor problems; mutant pups survive when fed separately, but 45 days after birth their body weight is only 50 to 60 % of that of wild-type (PubMed:11517255). They appear uncoordinated and display severe ataxia, myoclonus and spontaneous whole-body muscle jerks, but display no obvious alterations in brain morphology (PubMed:11517255, PubMed:15217387, PubMed:16923152). Mice lacking only Kcnc3 still display ataxic gait and decreased motor skill, but to a lesser degree than mice lacking both Kcnc3 and Kcnc1 (PubMed:16923152, PubMed:18448641). Purkinje cell-specific expression of Kcnc3 restores normal motor skills (PubMed:18448641). Mutant mice are also much more sensitive to ethanol and fall sideways at ethanol concentrations that have no effect on wild-type mice (PubMed:11517255). They display increased locomotor and exploratory activity (PubMed:11517255, PubMed:15217387). Mice lacking Kcnc3 or both Kcnc3 and Kcnc1 are resistant to the tremorogenic agent harmaline (PubMed:15217387). {ECO:0000269|PubMed:11517255, ECO:0000269|PubMed:15217387, ECO:0000269|PubMed:16923152, ECO:0000269|PubMed:18448641}. |