Referenced in: none

Automatically associated channels: TASK1

Title: Voltage-gated K(+) channels contributing to temporal precision at the inner hair cell-auditory afferent nerve fiber synapses in the mammalian cochlea.

Authors: Min-Ho Oak, Eunyoung Yi

Journal, date & volume: Arch. Pharm. Res., 2014 Jul , 37, 821-33

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/24925343

Abstract
To perform auditory tasks such as sound localization in the space, auditory neurons in the brain must distinguish sub-millisecond temporal differences in signals from two ears. Such high temporal resolution is possible when each neuron in the ascending auditory pathway fires brief action potential at very accurate timing. Various pre- and postsynaptic machineries ensuring such high temporal precision of auditory synaptic transmission have been identified. Of particular, in this review, the role of K(+) channels in shortening the duration of synaptic potentials will be discussed. First, the contribution of K(+) channels to AP firing of general auditory neurons will be discussed. Then, the focus will be moved to the inner hair cell (IHC)-auditory afferent nerve fiber (ANF) synapses, the first synapses of ascending auditory pathway. Molecular and immunohistological techniques have revealed various K(+) channels in the cell bodies and their processes of ANFs. Since the development of patch-clamp recordings from the ANF dendrites in 2002, it became possible to monitor the IHC-ANF synaptic transmission in greater detail. As revealed in brain auditory synapses, several different K(+) channels appear to participate in reducing the duration of synaptic potentials at the IHC-ANF synapses. In addition, K(+) channels at the ANF dendrites might act as potential targets of efferent feedback from the brain. The hypothesis is that, upon loud sound exposure, efferent neurotransmitters released onto the ANF dendrites activate certain K(+) channels and prevent excitotoxicity of ANFs. Therefore, K(+) channels of the ANF dendrites might provide potential sites of pharmacological actions to prevent noise-induced hearing loss.