Motin V G, Nikitin V P, Sherstnev V V
P. K. Anokhin Institute of Normal Physiology, Russian Academy of Medical Sciences, Moscow.
Bull Exp Biol Med. 2002 Feb;133(2):110-3. doi: 10.1023/a:1015518015515.
Effects of idiotypic and antiidiotypic antibodies against protein S100b on synaptic transmission and long-term potentiation of CA1 pyramidal neurons in rat hippocampus were studied. Idiotypic antibodies against protein S100b inhibited synaptic transmission from Schaffer collateral axons to pyramidal neurons, but had no effect on neuronal responses to antidromic stimulation. Antiidiotypic antibodies against protein S100b facilitated neuronal responses to orthodromic stimulation. Idiotypic antibodies against protein S100b suppressed changes in neuronal responses to orthodromic stimulation during long-term potentiation, while antiidiotypic antibodies facilitated these effects. Our findings suggest that the effects of idiotypic and antiidiotypic antibodies to protein S100b are associated with their regulatory influences on synaptic transmission. These mechanisms differ from mechanisms of synaptic plasticity involved in long-term potentiation.
研究了抗蛋白S100b的独特型抗体和抗独特型抗体对大鼠海马CA1锥体神经元突触传递和长时程增强的影响。抗蛋白S100b的独特型抗体抑制了从Schaffer侧支轴突到锥体神经元的突触传递，但对神经元对逆向刺激的反应没有影响。抗蛋白S100b的抗独特型抗体促进了神经元对顺向刺激的反应。抗蛋白S100b的独特型抗体在长时程增强过程中抑制了神经元对顺向刺激反应的变化，而抗独特型抗体则促进了这些效应。我们的研究结果表明，抗蛋白S100b的独特型抗体和抗独特型抗体的作用与其对突触传递的调节影响有关。这些机制不同于参与长时程增强的突触可塑性机制。
