Topic: auditory brainstem response

Adaptive myelination is the emerging concept of tuning axonal conduction velocity to the activity within specific neural circuits over time. Sound processing circuits process signals with microsecond precision: a time scale that is amenable to adjustment in length and thickness of myelin. Sound-evoked responses during postnatal development increase the activity of auditory axons and enhance myelin thickness, while sensory deprivation prevents such radial growth during development. Deprivation occurring during adulthood reduces myelin thickness. However, it is unclear if sensory stimulation adj

Aims: SCA13 patients carrying the R420H mutation in Kv3.3 also have compromised sound localization based on inferior processing of interaural differences in time and intensity of sound. These patients show no pure-tone deficit in the audiogram and their peripheral auditory system seems unaffected. The Kv3.3 subunit of voltage-gated potassium channels is highly expressed in fast-firing neurons of the auditory pathway, including the medial nucleus of the trapezoid body (MNTB) and the lateral superior olive (LSO) and is often co-expressed with the Kv3.1 subunit. Here, we investigate how this Kv3.

The auditory loss is associated with increased cognitive deterioration and even dementia, including Alzheimer's Disease (AD). However, the relation between the cause of the auditory loss and the mechanism during AD is still unknown. One hypothesis is that social isolation after hearing loss could facilitate dementia. Still, it is also believed that AD itself could cause alterations in the auditory pathway and this alteration promotes cognitive deterioration. The auditory signal is transmitted along the auditory pathway in the form of action potentials through the auditory nerve and across the