A Ca²⁺ level-independent component of recovery from sensory adaptation supports continuous vesicle supply at cochlear hair cell ribbon synapses.

IF 4.5 2区综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES

iScience Pub Date : 2026-09-30 eCollection Date: 2026-10-16 DOI:10.1016/j.isci.2026.117694

Walen L Gribaudo, Camila Catalano Di Meo, Lucía Agüero, Daniela Chequer Charan, Mark A Rutherford, Juan D Goutman

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引用次数: 0

Abstract

Maintenance of synaptic transmission can be accelerated by mechanisms dependent on intracellular Ca²⁺ signaling. However, at the first auditory synapse between sensory inner hair cells (IHCs) and spiral ganglion neurons (SGNs) in the cochlea, the process of synaptic vesicle recovery following strong, prolonged stimulation is unclear. To address this, we examined the Ca²⁺-dependence of presynaptic recovery in IHCs with measurements of postsynaptic activity in SGNs while depolarizing the IHC. Following vesicle-depleting stimulation of 1 second duration, SGN postsynaptic responses recovered completely within a few seconds. This process was unperturbed when reducing the intracellular Ca²⁺concentration by changing from 1 to 5 mM EGTA. Thus, synaptic recovery following depleting stimulation at IHC-SGN synapses may differ from the Ca²⁺-dependent process described during and after stimulation over shorter timescales. We propose a Ca²⁺ level-insensitive mechanism of recovery at this continuously active sensory synapse to support vesicle release rates of hundreds per second indefatigably.

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一种不依赖于水平的感觉适应恢复组分支持耳蜗毛细胞带状突触连续的囊泡供应。

突触传递的维持可以通过依赖于细胞内Ca2+信号传导的机制来加速。然而，在耳蜗感觉内毛细胞（IHCs）和螺旋神经节神经元（sgn）之间的第一听觉突触中，强烈、长时间刺激后突触囊泡恢复的过程尚不清楚。为了解决这个问题，我们在IHC去极化时，通过测量sgn的突触后活性，研究了IHC突触前恢复的Ca2+依赖性。在持续1秒的囊泡耗尽刺激后，SGN突触后反应在几秒钟内完全恢复。当通过改变1至5 mM EGTA来降低细胞内Ca2+浓度时，这一过程不受干扰。因此，IHC-SGN突触耗竭刺激后的突触恢复可能与较短时间内刺激期间和刺激后描述的Ca2+依赖过程不同。我们提出一种Ca2+水平不敏感的恢复机制，在这种持续活跃的感觉突触中支持每秒数百个囊泡的释放率。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

iScience Multidisciplinary-Multidisciplinary

CiteScore

7.20

自引率

1.70%

发文量

1972

审稿时长

6 weeks

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