Zhuo M, Zhang W, Son H, Mansuy I, Sobel R A, Seidman J, Kandel E R
Howard Hughes Medical Institute, Columbia University, New York, NY 10032, USA.
Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4650-5. doi: 10.1073/pnas.96.8.4650.
Pharmacological studies have suggested that long-term potentiation (LTP) and long-term depression (LTD) and depotentiation, three forms of synaptic plasticity in the hippocampus, require the activity of the phosphatase calcineurin. At least two different isoforms of calcineurin are found in the central nervous system. To investigate whether all of these forms of synaptic plasticity require the same isoforms of calcineurin, we have examined LTD, depotentiation, and LTP in mice lacking the predominant calcineurin isoform in the central nervous system, Aalpha-/- mice. Depotentiation was abolished completely whereas neither LTD nor LTP were affected. These studies provide genetic evidence that the Aalpha isoform of calcineurin is important for the reversal of LTP in the hippocampus and indicate that depotentiation and LTD operate through somewhat different molecular mechanisms.
药理学研究表明,长时程增强(LTP)、长时程抑制(LTD)和去增强作用,海马体中突触可塑性的三种形式,需要磷酸酶钙调神经磷酸酶的活性。在中枢神经系统中发现了至少两种不同的钙调神经磷酸酶同工型。为了研究是否所有这些形式的突触可塑性都需要相同的钙调神经磷酸酶同工型,我们检测了缺乏中枢神经系统中主要钙调神经磷酸酶同工型的小鼠(Aalpha-/-小鼠)的LTD、去增强作用和LTP。去增强作用完全消失,而LTD和LTP均未受影响。这些研究提供了遗传学证据,表明钙调神经磷酸酶的Aalpha同工型对海马体中LTP的逆转很重要,并表明去增强作用和LTD通过 somewhat 不同的分子机制起作用。 (注:原文中“somewhat”疑有误,结合语境这里应是“some”)