Sokolov Maxim V, Rossokhin Alexej V, M Kasyanov Alexander, Gasparini Sonia, Berretta Nicola, Cherubini Enrico, Voronin Leon L
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Butlerova str. 5a, 117865 Moscow, Russia.
Eur J Neurosci. 2003 Apr;17(7):1425-37. doi: 10.1046/j.1460-9568.2003.02563.x.
Whole cell recordings of excitatory postsynaptic potentials/currents (EPSPs/EPSCs) evoked by minimal stimulation of commissural-associative (CF) and mossy fibre (MF) inputs were performed in CA3 pyramidal neurons. Paired responses (at 50 ms intervals) were recorded before, during and after hyperpolarization of the postsynaptic membrane (20-30 mV for 15-35 min). Membrane hyperpolarization produced a supralinear increase of EPSPs/EPSCs amplitude in MF-inputs. Synaptic responses remained potentiated for the rest of the recording period (up to 40 min) after resetting the membrane potential to control level (221 +/- 60%, n = 15 and 219 +/- 61%, n = 11 for MF-EPSP and MF-EPSC, respectively). We shall refer to this effect as hyperpolarization-induced LTP (HI-LTP). In the absence of afferent stimulation, membrane hyperpolarization was unable to produce HI-LTP. In contrast to MF-EPSPs, the mean amplitude of CF-EPSPs did not increase significantly after hyperpolarization relative to controls (138 +/- 29%, n = 22). HI-LTP was associated with modifications of classical indices of presynaptic release: paired-pulse facilitation, failures rate, coefficient of variation of EPSP amplitudes and quantal content. The induction of HI-LTP was NMDA independent but was dependent on metabotropic glutamate receptors (mGluRs) activation and calcium release from inositol 1,4,5-triphosphate (IP3)-sensitive intracellular stores: it was prevented by mGluR antagonist, intracellular heparin and BAPTA. We conclude that while the induction of HI-LTP was postsynaptic, its expression was presynaptic.
在CA3锥体神经元中，对联合-联合（CF）和苔藓纤维（MF）输入进行最小刺激所诱发的兴奋性突触后电位/电流（EPSPs/EPSCs）进行全细胞记录。在突触后膜超极化（20 - 30 mV，持续15 - 35分钟）之前、期间和之后记录配对反应（间隔50毫秒）。膜超极化使MF输入中EPSPs/EPSCs的幅度呈超线性增加。在将膜电位重置为对照水平后，突触反应在记录期的其余时间（长达40分钟）保持增强（MF-EPSP和MF-EPSC分别为221±60%，n = 15和219±61%，n = 11）。我们将这种效应称为超极化诱导的长时程增强（HI-LTP）。在没有传入刺激的情况下，膜超极化无法产生HI-LTP。与MF-EPSPs相反，超极化后CF-EPSPs的平均幅度相对于对照没有显著增加（138±29%，n = 22）。HI-LTP与突触前释放的经典指标改变有关：配对脉冲易化、失败率、EPSP幅度的变异系数和量子含量。HI-LTP的诱导不依赖NMDA，但依赖代谢型谷氨酸受体（mGluRs）的激活以及从肌醇1,4,5-三磷酸（IP3）敏感的细胞内储存中释放钙：它被mGluR拮抗剂、细胞内肝素和BAPTA所阻断。我们得出结论：虽然HI-LTP的诱导是突触后性的，但其表达是突触前性的。
