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听觉病理学小鼠模型中梯形束内侧核的产后发育变化。

Postnatal developmental changes in the medial nucleus of the trapezoid body in a mouse model of auditory pathology.

机构信息

Department of Anatomy and Neurobiology, Northeast Ohio Medical University, Rootstown, OH 44272, United States.

Department of Anatomy and Neurobiology, Northeast Ohio Medical University, Rootstown, OH 44272, United States.

出版信息

Neurosci Lett. 2014 Jan 24;559:152-7. doi: 10.1016/j.neulet.2013.11.051. Epub 2013 Dec 6.

DOI:10.1016/j.neulet.2013.11.051
PMID:24315975
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3910105/
Abstract

Age-related hearing loss (AHL) is a multifactorial disorder characterized by a decline in peripheral and central auditory function. Here, we examined synaptic transmission in DBA/2 mice, which carry the AHL8 gene, at the identifiable glutamatergic synapse in the medial nucleus of the trapezoid body (MNTB), a nucleus in the superior olivary complex critical for acoustic timing. Mice exhibited raised auditory brainstem thresholds by P14, soon after hearing onset. Excitatory postsynaptic currents were prolonged; however, postsynaptic excitability was normal. By P18, high-frequency hearing loss was evident. Coincident with the onset of hearing loss, MNTB principal neurons displayed changes in intrinsic firing properties. These results suggest that changes in transmission in the superior olivary complex are associated with early onset hearing loss.

摘要

年龄相关性听力损失(AHL)是一种多因素疾病,其特征是外周和中枢听觉功能下降。在这里,我们研究了携带 AHL8 基因的 DBA/2 小鼠在中梯形核(MNTB)中的可识别谷氨酸能突触处的突触传递,MNTB 是上橄榄复合体中对声音计时至关重要的核。小鼠在 P14 时表现出听觉脑干阈值升高,这是在听力开始后不久。兴奋性突触后电流延长;然而,突触后兴奋性正常。到 P18 时,高频听力损失明显。与听力损失的开始同时,MNTB 主神经元显示出内在放电特性的变化。这些结果表明,上橄榄复合体中的传递变化与早期听力损失有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e8/3910105/707174d68546/nihms-547016-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e8/3910105/4d38ae42e8c7/nihms-547016-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e8/3910105/d077624083c1/nihms-547016-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e8/3910105/707174d68546/nihms-547016-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e8/3910105/4d38ae42e8c7/nihms-547016-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e8/3910105/d077624083c1/nihms-547016-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6e8/3910105/707174d68546/nihms-547016-f0003.jpg

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本文引用的文献

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抑制后反弹神经元和神经网络在逆转录病毒诱导的海绵状神经变性中受到破坏。
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Seizures and reduced life span in mice lacking the potassium channel subunit Kv1.2, but hypoexcitability and enlarged Kv1 currents in auditory neurons.缺乏钾通道亚基Kv1.2的小鼠会出现癫痫发作和寿命缩短的情况,但听觉神经元会出现兴奋性降低和Kv1电流增大的现象。
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