Reynolds T, Hartell N A
The Pharmaceutical Science Research Institute, Division of Life and Health Sciences, Aston University, Birmingham, UK.
Neuroreport. 2001 Jan 22;12(1):133-6. doi: 10.1097/00001756-200101220-00034.
In cerebellar slices conjunctive pairing of parallel fibre (PF) stimulation with depolarization of Purkinje cells (PCs) induces a long-term depression (LTD) of PF synaptic transmission that spreads to unpaired PF inputs to the same cell. Inhibitors of NO synthase (7-nitro-indazole), soluble guanylate cyclase (ODQ) and PKG (KT5823) all prevented depression at each of two independent PF pathways to a single PC. Inhibition of NOS also unmasked a platelet activating factor (PAF)-mediated synaptic potentiation of possible presynaptic origin. LTD was also prevented by the phospholipase A2 inhibitor OBAA but was rescued by co-perfusion with arachidonic acid. We conclude that NO and diffusible products of phospholipase A2 metabolism are potential mediators of the spread of cerebellar plasticity at the single cell level.
在小脑切片中，平行纤维（PF）刺激与浦肯野细胞（PC）去极化的联合配对可诱导PF突触传递的长时程抑制（LTD），该抑制会扩散到同一细胞的未配对PF输入。一氧化氮合酶抑制剂（7-硝基吲唑）、可溶性鸟苷酸环化酶（ODQ）和蛋白激酶G（KT5823）均能阻止在单个PC的两条独立PF通路中的每一条通路发生抑制。抑制一氧化氮合酶还揭示了一种可能源于突触前的血小板活化因子（PAF）介导的突触增强。磷脂酶A2抑制剂OBAA也能阻止LTD，但与花生四烯酸共同灌注可使其恢复。我们得出结论，一氧化氮和磷脂酶A2代谢的可扩散产物是小脑可塑性在单细胞水平扩散的潜在介质。
