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FMRF-NH2对药用水蛭心脏中间神经元之间高阈值传递的调节作用

Modulation of high-threshold transmission between heart interneurons of the medicinal leech by FMRF-NH2.

作者信息

Simon T W, Schmidt J, Calabrese R L

机构信息

Department of Biology, Emory University, Atlanta, Georgia 30322.

出版信息

J Neurophysiol. 1994 Feb;71(2):454-66. doi: 10.1152/jn.1994.71.2.454.

Abstract
  1. We examined high-threshold synaptic transmission between oscillatory pairs of leech heart interneurons. Inhibitory postsynaptic currents (IPSCs) could be reliably evoked by depolarizing the presynaptic neuron in voltage clamp from a holding potential of -35 mV. At this presynaptic potential, the Ca2+ currents underlying graded transmission are completely inactivated, and we conclude that a high-threshold Ca2+ current is extant in heart interneurons. Further evidence for this was that inhibitory postsynaptic currents were blocked when Co2+ replaced Ca2+ in the saline and thus high-threshold transmission was dependent on the presence of external Ca2+. 2. When IPSCs were evoked by a 200-ms duration voltage step from a holding potential of -35 mV in the presynaptic neuron, the time course of turn-on of the IPSC consisted of a fast (time-to-peak = 17.5 +/- 1.93 (SE) ms [n = 7]) and a slow (time-to-peak = 250 +/- 28.5 ms [n = 8]) component. FMRF-NH2 reduced the amplitude of the fast component but did not affect the slow component. When the presynaptic voltage step was ended the IPSC turned off with a single exponential time course. FMRF-NH2 slowed the time course of turn-off of the IPSC. 3. When IPSCs were evoked by a 1500-ms duration voltage step from a holding potential of -35 mV in the presynaptic neuron, these IPSCs peaked around 300 ms. Following the peak, the IPSC decayed with a single exponential time course. FMRF-NH2 accelerated the time course of this decay. At potentials of 0 mV and +5 mV, FMRF-NH2 produced a significant decrease in the peak current and at potentials of -5 mV and 0 mV, produced a significant decrease in the current integral. 4. High-threshold IPSCs could also be evoked by a spike in the presynaptic neuron. Bath application of 1 microM FMRF-NH2 decreased the amplitude of the spike-evoked IPSC and slowed the time course of its falling phase. 5. We examined the effect of FMRF-NH2 on the quantal synaptic transmission. Bath-application of FMRF-NH2 increased binomial p, the probability of release, and decreased binomial n, the number of units available for release. FMRF-NH2 had no effect on q, the unit size, when calculated from the distributions of PSPs, and increased the coefficient of variation (CV). 6. The lack of a change in q and the increase in CV suggested that FMRF-NH2 acted at a presynaptic location.(ABSTRACT TRUNCATED AT 400 WORDS)
摘要
  1. 我们研究了水蛭心脏中间神经元振荡对之间的高阈值突触传递。通过在电压钳中将突触前神经元从 -35 mV 的保持电位去极化,可可靠地诱发抑制性突触后电流(IPSC)。在这个突触前电位下,分级传递所依赖的 Ca2+ 电流完全失活,我们得出结论,心脏中间神经元中存在高阈值 Ca2+ 电流。进一步的证据是,当盐水中的 Co2+ 取代 Ca2+ 时,抑制性突触后电流被阻断,因此高阈值传递依赖于细胞外 Ca2+ 的存在。2. 当在突触前神经元中从 -35 mV 的保持电位通过 200 ms 持续时间的电压阶跃诱发 IPSC 时,IPSC 的开启时间进程包括一个快速成分(峰值时间 = 17.5 ± 1.93(标准误)ms [n = 7])和一个慢速成分(峰值时间 = 250 ± 28.5 ms [n = 8])。FMRF-NH2 降低了快速成分的幅度,但不影响慢速成分。当突触前电压阶跃结束时,IPSC 以单指数时间进程关闭。FMRF-NH2 减慢了 IPSC 的关闭时间进程。3. 当在突触前神经元中从 -35 mV 的保持电位通过 1500 ms 持续时间的电压阶跃诱发 IPSC 时,这些 IPSC 在约 300 ms 时达到峰值。峰值之后,IPSC 以单指数时间进程衰减。FMRF-NH2 加速了这种衰减的时间进程。在 0 mV 和 +5 mV 的电位下,FMRF-NH2 使峰值电流显著降低,在 -5 mV 和 0 mV 的电位下,使电流积分显著降低。4. 突触前神经元的一个动作电位也可诱发高阈值 IPSC。浴槽应用 1 μM FMRF-NH2 降低了动作电位诱发的 IPSC 的幅度,并减慢了其下降相的时间进程。5. 我们研究了 FMRF-NH2 对量子化突触传递的影响。浴槽应用 FMRF-NH2 增加了二项式 p,即释放概率,并降低了二项式 n,即可用于释放的单位数量。当根据 PSP 的分布计算时,FMRF-NH2 对 q,即单位大小,没有影响,并增加了变异系数(CV)。6. q 没有变化以及 CV 增加表明 FMRF-NH2 作用于突触前部位。(摘要截断于 400 字)

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