Popov V A, Markevich V A
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow.
Neurosci Behav Physiol. 2002 Nov-Dec;32(6):625-9. doi: 10.1023/a:1020413812499.
Experiments on rat hippocampal slices were performed with testing of the synaptic connections of Schaffer collaterals and neurons in field CA1 to study the effects of interrupting low-frequency test stimulation (0.05 Hz) on the amplitude of population spikes. These studies demonstrated a correlation between the duration of pauses in stimulation (form 10 to 120 min) and increases in the amplitude of spikes (on average by 30-100% of baseline response magnitude). This "deprivation" potentiation was additive and could persist for long periods of time (testing was up to 1 h). Preliminary induction of long-term post-tetanic potentiation, which prevented the subsequent development of the late, but not the shortterm phase, for 1-3 h, led to suppression of the development of "deprivation" potentiation after a 60-min pause in stimulation. Similar results were obtained in experiments using 20 microM polymyxin B, which blocks protein kinase C and the PKC-dependent phase of long-term post-tetanic potentiation; this is evidence supporting the previously advanced hypothesis that the development of deprivation potentiation and the late. PKC-dependent phase of long-term post-tetanic potentiation share common mechanisms, associated with people phosphorylation.
对大鼠海马切片进行了实验,测试了Schaffer侧支与CA1区神经元之间的突触连接,以研究中断低频测试刺激(0.05Hz)对群体峰电位幅度的影响。这些研究表明,刺激暂停的持续时间(从10到120分钟)与峰电位幅度的增加之间存在相关性(平均比基线反应幅度增加30 - 100%)。这种“剥夺”增强是累加性的,并且可以持续很长时间(测试长达1小时)。预先诱导长时程强直后增强,在刺激暂停60分钟后,该增强可在1 - 3小时内阻止后期而非短期阶段的后续发展,从而导致“剥夺”增强的发展受到抑制。在使用20微摩尔多粘菌素B的实验中也获得了类似结果,多粘菌素B可阻断蛋白激酶C以及长时程强直后增强的PKC依赖阶段;这一证据支持了先前提出的假说,即剥夺增强的发展与长时程强直后增强的后期PKC依赖阶段具有共同的机制,与蛋白质磷酸化有关。