Voltage-gated potassium (Kv) channels play a crucial role in regulating neuronal excitability by influencing the dynamics of repolarization during action potential (AP) generation, affecting their width, latency, and frequency. The Kv1.1 subunit has gained attention in neurobiological research due to its association with ataxia and increased epilepsy risk in humans with mutations in the KCNA1 gene. This thesis investigates the role of Kv1.1 in the murine auditory system, focusing on sound source location processing, which relies on precise AP generation and transmission. Mice encode azimuthal sound location through interaural intensity differences (IIDs) processed by lateral superior olive (LSO) neurons, which integrate excitatory and inhibitory inputs before relaying information to the inferior colliculus (IC). Electrophysiological recordings revealed limited IID sensitivity in LSO neurons to ipsilateral sound fields and reduced IID encoding efficiency due to increased temporal variability in inhibitory input. In the IC, Kv1.1 was found to be essential for maintaining latency disparities. Behavioral tests showed impaired sound location change detection in Kcna1-/- mice. The prepulse inhibition (PPI) paradigm demonstrated that while wild-type mice were affected by reduced IID availability, knockout mice could not utilize binaural cues effectively. This study highlights a general disruption in binaural integration in Kcna1-/- m
