| 268345 | Q14B80 | KCNC2_MOUSE | Potassium voltage-gated channel subfamily C member 2 (Shaw-like potassium channel) (Voltage-gated potassium channel Kv3.2) | DISRUPTION PHENOTYPE | Mice are healthy, grow normally, are fertile and show no evidence of severe sensory or motor abnormalities (PubMed:11124984). Show increased seizure susceptibility and reduced long-range synchronization of gamma oscillations over distance in the neocortex (PubMed:22539821). Thalamocortical neurons show a strong attenuation in maximal peak firing rates, with larger spikes and slower action potential repolarization (PubMed:17761775). Neocortical GABAergic interneurons display broader spikes and sustain lower trains of high-frequency spikes without accommodation or spike doublets in rapid succession (PubMed:11124984, PubMed:22539821). Histamine H2 receptor- and PKA-induced hippocampal inhibitory interneurons display no maximal sustainable firing frequency modulation (PubMed:10903572). Double knockout of KCNC2 and KCNC1 exhibited disrupted daily rhythms in wheel-running behavior (PubMed:21414897). Display smaller outward currents and slower deactivation in starburst amacrine cells compared with KCNC2 knockout mice (PubMed:15317859). Neocortical GABAergic interneuron terminals display also a reduced rate of spike repolarization, broader spike, increased calcium influx and release of GABA neurotransmitter (PubMed:15917463). Suprachiasmatic nucleus (SCN) neurons display a reduction in the magnitude of fast delayed rectifier potassium currents, wider action potentials, reduced spontaneous firing activity during the day and reduced NMDA-evoked increase firing responses during the night (PubMed:21414897). {ECO:0000269|PubMed:10903572, ECO:0000269|PubMed:11124984, ECO:0000269|PubMed:15317859, ECO:0000269|PubMed:15917463, ECO:0000269|PubMed:17761775, ECO:0000269|PubMed:21414897, ECO:0000269|PubMed:22539821}. |