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电压门控钾(K+)通道有助于哺乳动物耳蜗内毛细胞-听觉传入神经纤维突触的时间精度。

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

机构信息

College of Pharmacy and Natural Medicine Research Institute, Mokpo National University, 1666 Yeongsan-ro, Cheonggye-Myeon, Muan, Jeonnam, 534-729, Republic of Korea.

出版信息

Arch Pharm Res. 2014 Jul;37(7):821-33. doi: 10.1007/s12272-014-0411-8. Epub 2014 Jun 14.

DOI:10.1007/s12272-014-0411-8
PMID: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.

摘要

为了执行声音定位等听觉任务,大脑中的听觉神经元必须区分来自两耳的亚毫秒级时间差异信号。当上行听觉通路中的每个神经元以非常精确的时间发出短暂的动作电位时,就有可能实现这种高时间分辨率。已经确定了各种突触前和突触后机制,以确保听觉突触传递具有如此高的时间精度。特别是,在本次综述中,将讨论 K(+) 通道在缩短突触电位持续时间方面的作用。首先,将讨论 K(+) 通道对一般听觉神经元 AP 放电的贡献。然后,将注意力转移到内毛细胞 (IHC)-听觉传入神经纤维 (ANF) 突触上,这是上行听觉通路的第一个突触。分子和免疫组织化学技术已经揭示了 ANF 细胞体及其过程中的各种 K(+) 通道。自 2002 年从 ANF 树突进行膜片钳记录以来,有可能更详细地监测 IHC-ANF 突触传递。正如在脑听觉突触中所揭示的那样,几种不同的 K(+) 通道似乎参与了缩短 IHC-ANF 突触处突触电位的持续时间。此外,ANF 树突上的 K(+) 通道可能作为来自大脑的传出反馈的潜在靶点。该假设是,在强声暴露下,释放到 ANF 树突上的传出神经递质激活某些 K(+) 通道,防止 ANF 的兴奋性毒性。因此,ANF 树突上的 K(+) 通道可能为预防噪声性听力损失提供潜在的药物作用部位。

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