Impact of synaptic depression on spike timing at the endbulb of Held

突触抑制对赫尔德终球动作电位时序的影响

阅读:1

Abstract

Many synapses show short-term depression, but it is not well understood what functional purpose depression serves and whether its effects are beneficial or detrimental to information processing. We study this issue at the synapse made by auditory-nerve (AN) fibers onto bushy cells (BCs) of the cochlear nucleus, called the "endbulb of Held." AN fibers carry timing information about sounds and converge on BCs, which relay timing information to brain areas responsible for sound localization. Dynamic-clamp recordings of BCs in mouse brain slices indicated that nonphase-locked inputs influenced the contribution of phase-locked inputs when all inputs had equal strength. We evaluated whether this situation depended on activity-dependent synaptic plasticity. Voltage-clamp recordings indicated that the amount of depression varied over the population of endbulbs, but sibling endbulbs terminating on the same BC had similar plasticity. We tested the effects of endbulb depression on BC spiking using dynamic clamp. Under most conditions, increasing depression led to lower probability of BC spiking. However, the effects on spike timing were highly context dependent. When all inputs carried uniform timing information, depression indirectly affected BC spike precision, by determining how many inputs were required to cross threshold. Earlier work has indicated that this interacts with the temporal distribution of inputs to determine BC spike precision. When inputs carried different timing information, depression greatly improved BC precision by suppressing highly active inputs carrying little phase-locked information. These data suggest that endbulbs with different depression characteristics could produce BCs that enhance response probability or timing under different stimulus conditions.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。