Modulation of high-threshold transmission between heart interneurons of the medicinal leech by FMRF-NH2.
Modulation of high-threshold transmission between heart interneurons of the medicinal leech by FMRF-NH2.
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FMRF-NH2 对药用水蛭心脏中间神经元之间高阈值传输的调节。
DOI：
10.1152/jn.1994.71.2.454
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发表时间：
1994
影响因子：
2.5
通讯作者：
Calabrese,RL
中科院分区：
文献类型：
--
作者：
Simon,TW;Schmidt,J;Calabrese,RL
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。在电压钳技术中，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，Ca 2+电流的基础上分级传输完全失活，我们得出结论，高阈值Ca 2+电流是现存的心脏中间神经元。进一步的证据是，抑制性突触后电流被阻止时，钴2+取代的Ca 2+在盐水中，因此高阈值传输依赖于外部Ca 2+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开启的时间过程由快（达峰时间= 17.5 +/- 1.93（SE）ms [n = 7]）和慢（达峰时间= 250 +/- 28.5 ms [n = 8]）分量组成。FMRF-NH 2降低了快成分的幅度，但不影响慢成分。当突触前电压阶跃结束时，IPSC以单指数时间过程关闭。FMRF-NH 2减缓了IPSC关闭的时间过程。3.当突触前神经元的保持电位为-35 mV，持续1500 ms的电压阶跃诱发IPSC时，这些IPSC在300 ms左右达到峰值。峰值之后，IPSC以单指数时间过程衰减。FMRF-NH 2加速了这种衰减的时间过程。在0 mV和+5 mV的电位下，FMRF-NH 2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.高阈值IPSC也可以由突触前神经元中的尖峰诱发。浴用1 μ M FMRF-NH_2降低了棘波诱发的IPSC的幅度，并减慢了其下降相的时程。5.我们研究了FMRF-NH 2对量子突触传递的影响。FMRF-NH 2的重复施用增加了二项式p，释放的概率，并降低了二项式n，可用于释放的单位数。FMRF-NH 2对从PSP分布计算的单位大小q没有影响，并增加了变异系数（CV）。6.缺乏q的变化和CV的增加表明FMRF-NH 2作用于突触前位置。（400字处截断摘要）
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)