Sound Localization in Preweanling Mice Was More Severely Affected by Deleting the Kcna1 Gene Compared to Deleting Kcna2 , and a Curious Inverted-U Course of Development That Appeared to Exceed Adult Performance Was Observed in All Groups

AbstractThe submillisecond acuity for detecting rapid spatial and temporal fluctuations in acoustic stimuli observed in humans and laboratory animals depends in part on select groups of auditory neurons that preserve synchrony from the ears to the binaural nuclei in the brainstem. These fibers have specialized synapses and axons that use a low-threshold voltage-activated outward current,IKL, conducted through Kv1 potassium ion channels. These are in turn coupled with HCN channels that express a mixed cation inward mixed current,IH, to support precise synchronized firing. The behavioral evidence is that their respectiveKcna1 orHCN1 genes are absent in adult mice; the results are weak startle reflexes, slow responding to noise offsets, and poor sound localization. The present behavioral experiments were motivated by an in vitro study reportingincreased IKL in an auditory nucleus inKcna2−/− mice lacking the Kv1.2 subunit, suggesting thatKcna2−/− mice might perform better thanKcna2+/+ mice. BecauseKcna2−/− mice have only a 17 –18-day lifespan, we compared both preweanlingKcna2−/− vs.Kcna2+/+ mice andKcna1−/− vs.Kcna1+/+ mice at P12-P17/18; then, the remaining mice were tested at P23/P25. Both null mutant strains had a stunted physique, but theKcna1−/− mice had severe behavioral deficits while those inKcna2−/− mice were relatively few and minor. The in vitro increase ofIKL could have resulted from Kv1.1 subunits substituting for Kv1.2  units and the ...
Source: JARO - Journal of the Association for Research in Otolaryngology - Category: ENT & OMF Source Type: research