Gardner D
J Neurophysiol. 1986 Nov;56(5):1424-38. doi: 10.1152/jn.1986.56.5.1424.
In order to examine the relative contributions of changes in amplitude and time course to synaptic plasticity, variations in peak amplitude and time constant of decay have been analyzed from inhibitory postsynaptic currents (PSC) recorded in voltage-clamped Aplysia buccal ganglia neurons. In these cells, synaptic currents with single time constant decay can be recorded with low noise under well-controlled space clamp. Over a population of 36 neurons, duration was more narrowly distributed than amplitude, but each varied. The coefficient of variation (CV) was 0.21 for decay time constant (tau) and 0.87 for peak conductance (g peak). Population variances are larger than can be accounted for by such variables as temperature and noise amplitude, suggesting that functional modifications alter each of these determinants of synaptic effectiveness over the long term. Recordings of up to several hundred PSC in each of 16 neurons show that both PSC amplitude and time course recorded in a single cell can vary independently over short time spans. Decay remained single exponential as time course changed. CV for tau averaged 0.11; CV for g peak was 0.19. Variability of tau was not an artifact of amplitude; CV was relatively uncorrelated with current amplitudes or sample size. Smoothing and adding excess noise to each individual PSC of a set produced only small changes to CV, showing that variability was not an artifact of noise. Several specific manipulations of the presynaptic neuron altered both PSC amplitude and time course. Tetanic stimulation of the presynaptic neuron produced short-term potentiation of both amplitude and time course of subsequent PSCs. Peak amplitude was increased by 80%; tau by 12%. Reducing interspike intervals from 10 to 1 s produced habituation of both amplitude and time course, with g peak decreasing by 35 to 40% and tau by 10%. Conditioning DC depolarization of the presynaptic neuron enhanced PSC amplitude with little effect on decay time constant. Although short-term plastic changes affect PSC amplitude more than duration, each is alterable. Parallel changes in both can synergistically alter synaptic charge transfer, and therefore efficacy. Similar mechanisms may produce larger long-term differences seen between neurons.
为了研究幅度变化和时间进程对突触可塑性的相对贡献,我们分析了在电压钳制的海兔颊神经节神经元中记录到的抑制性突触后电流(PSC)的峰值幅度和衰减时间常数的变化。在这些细胞中,可以在良好控制的空间钳制下以低噪声记录具有单时间常数衰减的突触电流。在36个神经元群体中,持续时间的分布比幅度更窄,但两者均有变化。衰减时间常数(tau)的变异系数(CV)为0.21,峰值电导(g峰值)的变异系数为0.87。群体方差大于由温度和噪声幅度等变量所能解释的范围,这表明功能修饰会长期改变这些突触效能的决定因素中的每一个。在16个神经元中的每一个中记录多达数百个PSC,结果表明在单个细胞中记录到的PSC幅度和时间进程在短时间跨度内都可以独立变化。随着时间进程的改变,衰减保持单指数形式。tau的CV平均为0.11;g峰值的CV为0.19。tau的变异性不是幅度的假象;CV与电流幅度或样本大小相对不相关。对一组中的每个单独的PSC进行平滑处理并添加过量噪声只会使CV产生微小变化,这表明变异性不是噪声的假象。对突触前神经元进行的几种特定操作改变了PSC幅度和时间进程。对突触前神经元的强直刺激会使后续PSC的幅度和时间进程产生短期增强。峰值幅度增加了80%;tau增加了12%。将峰间间隔从10秒减少到1秒会使幅度和时间进程都产生习惯化,g峰值降低35%至40%,tau降低10%。对突触前神经元进行条件性直流去极化会增强PSC幅度,而对衰减时间常数影响很小。尽管短期可塑性变化对PSC幅度的影响大于持续时间,但两者均可改变。两者的平行变化可以协同改变突触电荷转移,进而改变效能。类似的机制可能会在神经元之间产生更大的长期差异。