PAIRING OF PRESYNAPTIC AND POSTSYNAPTIC ACTIVITIES IN CEREBELLAR PURKINJE-CELLS INDUCES LONG-TERM CHANGES IN SYNAPTIC EFFICACY INVITRO
PAIRING OF PRESYNAPTIC AND POSTSYNAPTIC ACTIVITIES IN CEREBELLAR PURKINJE-CELLS INDUCES LONG-TERM CHANGES IN SYNAPTIC EFFICACY INVITRO
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DOI：
10.1113/jphysiol.1991.sp018380
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发表时间：
1991-01-01
影响因子：
5.5
通讯作者：
JAILLARD, D
中科院分区：
文献类型：
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作者：
CREPEL, F;JAILLARD, D
1. 大鼠小脑皮质的体外切片制备被用来分析突触传递在平行纤维（PF）-浦肯野细胞（PC）突触的持久的修改。 这些使用依赖性的变化是通过配对PF介导的EPSP诱发的低频（1 Hz）与不同水平的膜极化（或生物电活动）的PC的15分钟。 实验在常规灌注室中细胞内记录的48个PC上进行，并且在存在（n = 21）或不存在（n = 29）400 nM-phorbol 12，13-dibutyrate（PDBu）的情况下在静态室中维持的50个其他细胞中进行。 在这三种实验条件下，PF介导的EPSP总是在保持电位为-75 mV的PC上测量，并通过恒定的超极化脉冲进一步超极化。 这使得我们既可以测试PC的输入电阻，又可以避免它们在PF介导的EPSP中放电。 在本研究所保留的所有细胞中，0.2Hz诱发的PF介导的EPSP的振幅在配对前阶段是稳定的，其振幅和时程也是如此。 在灌注室中，配对PF介导的EPSP与用于测量突触反应的PC相同的超极化对30%的PC中的EPSP没有影响。 分别在23%和47%的受试细胞中诱导长时程抑制（LTD）和长时程增强（LTP）（n = 17）. 在灌注室中，配对PF介导的EPSP与PC的中度去极化（n = 19）引起持续放电的钠峰显着有利于LTP的外观相比，以前的配对协议。 然而，仍有27%的细胞未显示修饰，15%的细胞显示LTD。 相比之下，配对PF介导的EPSP与由PC的强去极化诱发的钙（Ca 2+）尖峰（n = 12）导致近一半的测试细胞中的突触传递的LTD，而现在在不到20%的细胞中观察到LTP。 在静态室中，在没有PDBu的情况下，在大多数细胞中观察到PF介导的EPSP的LTD，无论与钠或Ca 2+尖峰的配对方案如何。 在使用钠尖峰放电的配对方案中，PDBu显著逆转了这种向LTD的转变，但在与Ca 2+尖峰配对的情况下并非如此。 无论使用何种方案，长时程突触变化并不伴随着细胞输入电阻或EPSP潜伏期的任何显着变化。 在所有情况下，LTP和LTD都伴随着PF介导的EPSP初始斜率的增加和减少。 这些结果与以前的研究结果一起表明，PF-PC突触LTP的诱导至少部分是突触前的，并且可以通过蛋白激酶C的直接激活而增加。 他们还认为，PC可以加强这种LTP，或者可以将其转化为LTD，这取决于它们对钠或Ca 2+尖峰的激发。
1. An in vitro slice preparation of rat cerebellar cortex was used to analyse long-lasting modifications of synaptic transmission at parallel fibre (PF)-Purkinje cell (PC) synapses. These use-dependent changes were induced by pairing PF-mediated EPSPs evoked at low frequency (1 Hz) with different levels of membrane polarization (or bioelectrical activities) of PCs for 15 min.2. Experiments were performed on forty-eight PCs recorded intracellularly in a conventional perfused chamber, and in fifty other cells maintained in a static chamber either in the presence (n = 21) or in the absence (n = 29) of 400 nM-phorbol 12,13-dibutyrate (PDBu).3. In these three experimental conditions, PF-mediated EPSPs were always measured on PCs maintained at a holding potential of -75 mV, and further hyperpolarized by constant hyperpolarizing pulses. This allowed us both to test the input resistance of PCs and to avoid their firing during PF-mediated EPSPs.4. In all cells retained for the present study, latencies of PF-mediated EPSPs evoked at 0.2 Hz were stable during the pre-pairing period, and the same was true for their amplitude and time course.5. In the perfused chamber, pairing of PF-mediated EPSPs with the same hyperpolarization of PCs as that used for measurements of synaptic responses had no effect on these EPSPs in 30% of PCs. It induced long-term depression (LTD) and long-term potentiation (LTP) in 23 and 47% of the tested cells respectively (n = 17).6. In the perfused chamber, pairing of PF-mediated EPSPs with moderate depolarization of PCs (n = 19) giving rise to a sustained firing of sodium spikes significantly favoured the appearance of LTP as compared to the previous pairing protocol. However, there were still 27 and 15% of cells which showed no modification and LTD respectively.7. In contrast, pairing of PF-mediated EPSPs with calcium (Ca2+) spikes evoked by strong depolarization of PCs (n = 12) led to LTD of synaptic transmission in nearly half of the tested cells, whereas LTP was now observed in less than 20% of them.8. In the static chamber and in the absence of PDBu, LTD of PF-mediated EPSPs was observed in most cells, whatever the pairing protocol with sodium or Ca2+ spikes.9. This shift towards LTD was significantly reversed by PDBu in the pairing protocol using firing of sodium spikes, but not in the case of pairings with Ca2+ spikes.10. Whatever the protocol used, long-term synaptic changes were not accompanied by any significant variation of cell input resistance or latency of EPSPs. In all cases, LTP and LTD were accompanied by increase and decrease of the initial slope of PF-mediated EPSPs.11. These results, together with those from previous studies, suggest that induction of LTP at PF-PC synapses is at least partly presynaptic and can be increased by direct activation of protein kinase C. They also suggest that PCs can reinforce this LTP or alternatively can convert it into LTD depending on their firing on sodium or Ca2+ spikes.