A rapid form of activity-dependent recovery from short-term synaptic depression in the intensity pathway of the auditory brainstem.
A rapid form of activity-dependent recovery from short-term synaptic depression in the intensity pathway of the auditory brainstem.
复制标题
听觉脑干强度通路中短期突触抑制的一种快速的活动依赖性恢复形式。
DOI：
10.1007/s00422-011-0428-8
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发表时间：
2011
影响因子：
1.9
通讯作者：
Horiuchi,TimothyK
中科院分区：
文献类型：
--
作者：
MacLeod,KatrinaM;Horiuchi,TimothyK
短期突触可塑性作为一个时间和发射率依赖的过滤器，介导的信息传输突触。在鸟类听觉脑干中，特定形式的可塑性在相同的听觉神经纤维的不同末端表达，并有助于声音时间和强度信息的发散。为了确定可塑性特性的关键差异，我们从耳蜗核负责强度编码的神经元（角核）进行膜片钳记录，并测量了短期突触抑制后兴奋性突触后电流恢复的时间过程。这些突触反应显示出非常快速的恢复，遵循双指数时间过程，具有~40 ms的快速时间常数和对突触前活动水平的依赖性，导致在高速率与低速率刺激序列之后的恢复轨迹交叉。我们还表明，强度通路中记录的恢复与时间通路中的类似记录不同，特别是耳蜗大细胞核，在两个方面：（1）快速恢复不是由于从突触后受体脱敏中恢复，以及（2）以非单调隆起为特征的恢复轨迹，这可能部分是由于强度通路中更普遍的易化机制。我们测试了先前提出的基于囊泡耗尽和囊泡补充的顺序步骤的突触传递模型是否可以解释恢复反应，并发现它是不够的，这表明存在活性依赖性反馈机制。我们建议，抑郁症后的快速恢复可以改善自然听觉信号的编码，这些信号通常由短间隙分隔的声音突发组成。
Short-term synaptic plasticity acts as a time- and firing rate-dependent filter that mediates the transmission of information across synapses. In the avian auditory brainstem, specific forms of plasticity are expressed at different terminals of the same auditory nerve fibers and contribute to the divergence of acoustic timing and intensity information. To identify key differences in the plasticity properties, we made patch-clamp recordings from neurons in the cochlear nucleus responsible for intensity coding, nucleus angularis, and measured the time course of the recovery of excitatory postsynaptic currents following short-term synaptic depression. These synaptic responses showed a very rapid recovery, following a bi-exponential time course with a fast time constant of ~40 ms and a dependence on the presynaptic activity levels, resulting in a crossing over of the recovery trajectories following high-rate versus low-rate stimulation trains. We also show that the recorded recovery in the intensity pathway differs from similar recordings in the timing pathway, specifically the cochlear nucleus magnocellularis, in two ways: (1) a fast recovery that was not due to recovery from postsynaptic receptor desensitization and (2) a recovery trajectory that was characterized by a non-monotonic bump that may be due in part to facilitation mechanisms more prevalent in the intensity pathway. We tested whether a previously proposed model of synaptic transmission based on vesicle depletion and sequential steps of vesicle replenishment could account for the recovery responses, and found it was insufficient, suggesting an activity-dependent feedback mechanism is present. We propose that the rapid recovery following depression allows improved coding of natural auditory signals that often consist of sound bursts separated by short gaps.