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首页> 外文期刊>The European Journal of Neuroscience >Functional implications of Ca(v)2.3 R-type voltage-gated calcium channels in the murine auditory system - novel vistas from brainstem-evoked response audiometry
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Functional implications of Ca(v)2.3 R-type voltage-gated calcium channels in the murine auditory system - novel vistas from brainstem-evoked response audiometry

机译：CA（v）2.3 r型电压门控钙通道在鼠听觉系统中的功能影响 - 从脑干诱发的响应听力学中的新型Vistas

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摘要

Voltage-gated Ca2+ channels (VGCCs) are considered to play a key role in auditory perception and information processing within the murine inner ear and brainstem. In the past, Ca(v)1.3 L-type VGCCs gathered most attention as their ablation causes congenital deafness. However, isolated patch-clamp investigation and localization studies repetitively suggested that Ca(v)2.3 R-type VGCCs are also expressed in the cochlea and further components of the ascending auditory tract, pointing to a potential functional role of Ca(v)2.3 in hearing physiology. Thus, we performed auditory profiling of Ca(v)2.3(+/+) controls, heterozygous Ca(v)2.3(+/-) mice and Ca(v)2.3 null mutants (Ca(v)2.3(-/-)) using brainstem-evoked response audiometry. Interestingly, click-evoked auditory brainstem responses (ABRs) revealed increased hearing thresholds in Ca(v)2.3(+/-) mice from both genders, whereas no alterations were observed in Ca(v)2.3(-/-) mice. Similar observations were made for tone burst-related ABRs in both genders. However, Ca(v)2.3 ablation seemed to prevent mutant mice from total hearing loss particularly in the higher frequency range (36-42 kHz). Amplitude growth function analysis revealed, i.a., significant reduction in ABR wave W-I and W-III amplitude in mutant animals. In addition, alterations in W-I-W-IV interwave interval were observed in female Ca(v)2.3(+/-) mice whereas absolute latencies remained unchanged. In summary, our results demonstrate that Ca(v)2.3 VGCCs are mandatory for physiological auditory information processing in the ascending auditory tract.
机译：电压门控CA2 +通道（VGCC）被认为在鼠内耳和脑干内的听觉感知和信息处理中发挥关键作用。过去，CA（v）1.3 L-型VGCC在他们的消融导致先天性耳聋时聚集了最受关注的。然而，分离的蛋白钳调查和本地化研究重复地表明Ca（v）2.3 r型VGCC也在耳蜗和升序的进一步成分中表达，指向Ca（v）2.3的潜在功能作用听力生理学。因此，我们对Ca（v）2.3（+ / +）对照，杂合性Ca（v）2.3（+/-）小鼠和Ca（v）2.3氟突变体（Ca（v）2.3（ - / - ）进行检测分析）使用脑干诱发的响应听力测定。有趣的是，点击诱发的听觉脑干响应（ABR）揭示了来自两者的Ca（v）2.3（+/-）小鼠中增加的听力阈值，而在Ca（v）2.3（ - / - ）小鼠中没有观察到改变。在两个人中，对色调突发相关的ABR进行类似的观察。然而，Ca（v）2.3消融似乎在较高频率范围（36-42kHz）中，从总听力损失中防止突变小鼠。振幅生长函数分析显示，I.A.，突变动物中的ABR波W-I和W-III振幅显着降低。此外，在雌性Ca（v）2.3（+/-）小鼠中观察到W-I-W-IV次间隔内的改变，而绝对延迟保持不变。总之，我们的结果表明，CA（v）2.3 VGCC对于升上听觉道中的生理听觉信息处理是强制性的。

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