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首页> 外文期刊>Neuron >Parvalbumin-Interneuron Output Synapses Show Spike-Timing-Dependent Plasticity that Contributes to Auditory Map Remodeling
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Parvalbumin-Interneuron Output Synapses Show Spike-Timing-Dependent Plasticity that Contributes to Auditory Map Remodeling

机译:Parvalbumin-Interneuron输出突触显示有助于听觉地图重塑的峰值定时依赖性可塑性

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摘要

Parvalbumin (PV)-expressing interneurons mediate fast inhibition of principal neurons in many brain areas; however, long-term plasticity at PV-interneuron output synapses has been less well studied. In the auditory cortex, thalamic inputs drive reliably timed action potentials (APs) in principal neurons and PV-interneurons. Using paired recordings in the input layer of the mouse auditory cortex, we found a marked spike-timing-dependent plasticity (STDP) at PV-interneuron output synapses. Long-term potentiation of inhibition (iLTP) is observed upon postsynaptic (principal neuron) then presynaptic (PV-interneuron) AP firing. The opposite AP order causes GABAB-mediated long-term depression of inhibition (iLTD), which is developmentally converted to iLTP in an experience-dependent manner. Genetic deletion of GABABreceptors in principal neurons suppressed iLTD and produced deficits in auditory map remodeling. Output synapses of PV-interneurons thus show marked STDP, and one limb of this plasticity, GABAB-dependent iLTD, is a candidate mechanism for disinhibition during auditory critical period plasticity.
机译:Parvalbumin(PV)-Expring Interneurons在许多脑区中介绍了主要神经元的快速抑制;然而,PV-Interneuron输出突触的长期可塑性已经不太良好地研究。在听觉皮质中,丘脑输入在主要神经元和PV型中达到可靠定时的动作电位(APS)。在鼠标听觉皮质的输入层中使用配对录制,我们发现了PV-Interneuron输出突触的标记的峰值定时依赖性可塑性(STDP)。在突触后(主要神经元)上观察到抑制的长期增强(ILLTP),然后在突触前(PV-Interneuron)AP烧制。相对的AP顺序导致加法布介导的抑制(ILTD)的长期抑制,其以经验依赖性的方式显影转化为ILTP。主要神经元中的Gababrecoper的遗传缺失抑制了ILTD并产生了听觉地图重塑中的缺陷。因此,PV-Interneurons的输出突触显示标记为STDP,并且这种可塑性的一个肢体,Gabab依赖性ILTD是在听觉关键时期可塑性期间解读的候选机构。

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