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首页> 外文期刊>The European Journal of Neuroscience >Spike-timing-dependent plasticity at resting and conditioned lateral perforant path synapses on granule cells in the dentate gyrus: different roles of N-methyl-D-aspartate and group I metabotropic glutamate receptors.
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Spike-timing-dependent plasticity at resting and conditioned lateral perforant path synapses on granule cells in the dentate gyrus: different roles of N-methyl-D-aspartate and group I metabotropic glutamate receptors.

机译：在齿状回的颗粒细胞上静息和条件性侧穿孔路径突触时，取决于尖峰时序的可塑性：N-甲基-D-天冬氨酸和I类代谢型谷氨酸受体的不同作用。

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We examined the mechanisms underlying spike-timing-dependent plasticity induction at resting and conditioned lateral perforant pathway (LPP) synapses in the rat dentate gyrus. Two stimulating electrodes were placed in the outer third of the molecular layer and in the granule cell layer in hippocampal slices to evoke field excitatory postsynaptic potentials (fEPSPs) and antidromic field somatic spikes (afSSs), respectively. Long-term potentiation (LTP) of LPP synapses was induced by paired stimulation with fEPSP preceding afSS. Reversal of the temporal order of fEPSP and afSS stimulation resulted in long-term depression (LTD). Induction of LTP or LTD was blocked by D,L-2-amino-5-phosphonopentanoic acid (AP5), showing that both effects were N-methyl-D-aspartate receptor (NMDAR)-dependent. Induction of LTP was also blocked by inhibitors of calcium-calmodulin kinase II, protein kinase C or mitogen-activated/extracellular-signal regulated kinase, suggesting that these are downstream effectors of NMDAR activation, whereas induction of LTD was blocked by inhibitors of protein kinase C and protein phosphatase 2B. At LPP synapses previously potentiated by high-frequency stimulation or depressed by low-frequency stimulation, paired fEPSP-afSS stimulation resulted in 'de-depression' at depressed LPP synapses but had no effect on potentiated synapses, whereas reversal of the temporal order of fEPSP-afSS stimulation resulted in 'de-potentiation' at potentiated synapses but had no effect on depressed synapses. Induction of de-depression and de-potentiation was unaffected by ap5 but was blocked by 2-methyl-6-(phenylethynyl) pyridine hydrochloride, a group I metabotropic glutamate receptor blocker, showing that both were NMDAR-independent but group I metabotropic glutamate receptor-dependent. In conclusion, our results show that spike-timing-dependent plasticity can occur at both resting and conditioned LPP synapses, its induction in the former case being NMDAR-dependent and, in the latter, group I metabotropic glutamate receptor-dependent.
机译：我们研究了在大鼠齿状回的静息和条件性侧穿孔通路（LPP）突触中潜在的依赖于穗期的可塑性诱导的机制。将两个刺激电极分别置于分子层的外部三分之一和海马切片的颗粒细胞层中，以分别引起场兴奋性突触后电位（fEPSPs）和反体场体突波（afSSs）。在afSS之前，通过与fEPSP配对刺激来诱导LPP突触的长期增强（LTP）。 fEPSP和afSS刺激的时间顺序逆转导致长期抑郁（LTD）。 LTP或LTD的诱导被D，L-2-氨基-5-膦基戊酸（AP5）阻断，表明这两种作用都是N-甲基-D-天冬氨酸受体（NMDAR）依赖性的。 LTP的诱导也被钙钙调蛋白激酶II，蛋白激酶C或有丝分裂原激活/细胞外信号调节激酶的抑制剂所阻断，这表明它们是NMDAR激活的下游效应子，而LTD的诱导被蛋白激酶的抑制剂所阻断。 C和蛋白磷酸酶2B。在先前通过高频刺激增强或通过低频刺激抑制的LPP突触中，成对的fEPSP-afSS刺激导致LPP突触的“降低”，但对增强的突触没有影响，而fEPSP的时间顺序逆转-afSS刺激在增强的突触中导致“去势增强”，但对抑制的突触没有影响。 ap5不影响诱导抑郁和去电位的作用，但被I-代谢型谷氨酸受体阻滞剂2-甲基-6-（苯基乙炔基）吡啶盐酸盐阻断，表明两者均不依赖NMDAR，但I组代谢型谷氨酸受体。 -依赖。总之，我们的结果表明，在静息LPP和条件LPP突触中都可能出现依赖于尖峰时序的可塑性，在前一种情况下，其诱导是NMDAR依赖性的，在后一种情况下，其诱导是I组代谢型谷氨酸受体的依赖性。

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