Sanchez Jason Tait, Quinones Karla, Otto-Meyer Sebastian
Roxelyn and Richard Pepper Department of Communication Sciences and Disorders, The Hugh Knowles Hearing Research Center, School of Communication, Northwestern University, Evanston, IL, USA. ; Department of Neurobiology and Interdepartmental Neuroscience Program, Northwestern University, Evanston, IL, USA.
Roxelyn and Richard Pepper Department of Communication Sciences and Disorders, The Hugh Knowles Hearing Research Center, School of Communication, Northwestern University, Evanston, IL, USA.
J Exp Neurosci. 2015 Oct 22;9(Suppl 2):11-24. doi: 10.4137/JEN.S25472. eCollection 2015.
Defined as reduced neural responses during high rates of activity, synaptic depression is a form of short-term plasticity important for the temporal filtering of sound. In the avian cochlear nucleus magnocellularis (NM), an auditory brainstem structure, mechanisms regulating short-term synaptic depression include pre-, post-, and extrasynaptic factors. Using varied paired-pulse stimulus intervals, we found that the time course of synaptic depression lasts up to four seconds at late-developing NM synapses. Synaptic depression was largely reliant on exogenous Ca(2+)-dependent probability of presynaptic neurotransmitter release, and to a lesser extent, on the desensitization of postsynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptor (AMPA-R). Interestingly, although extrasynaptic glutamate clearance did not play a significant role in regulating synaptic depression, blocking glutamate clearance at early-developing synapses altered synaptic dynamics, changing responses from depression to facilitation. These results suggest a developmental shift in the relative reliance on pre-, post-, and extrasynaptic factors in regulating short-term synaptic plasticity in NM.
突触抑制被定义为在高活动率期间神经反应减弱,它是一种短期可塑性形式,对声音的时间滤波很重要。在鸟类延髓听觉神经核(NM),一种听觉脑干结构中,调节短期突触抑制的机制包括突触前、突触后和突触外因素。使用不同的配对脉冲刺激间隔,我们发现,在发育较晚的NM突触中,突触抑制的时间进程持续长达四秒。突触抑制在很大程度上依赖于突触前神经递质释放的外源性钙依赖性概率,在较小程度上依赖于突触后α-氨基-3-羟基-5-甲基-4-异恶唑丙酸型谷氨酸受体(AMPA-R)的脱敏。有趣的是,虽然突触外谷氨酸清除在调节突触抑制中不起重要作用,但在发育早期的突触中阻断谷氨酸清除会改变突触动力学,使反应从抑制变为易化。这些结果表明,在调节NM短期突触可塑性时,突触前、突触后和突触外因素的相对依赖性存在发育转变。