一种关于学习和记忆背后的赫布与反赫布过程的机制。
A mechanism for the Hebb and the anti-Hebb processes underlying learning and memory.
作者信息
Lisman J
机构信息
Department of Biology, Brandeis University, Waltham, MA 02254.
出版信息
Proc Natl Acad Sci U S A. 1989 Dec;86(23):9574-8. doi: 10.1073/pnas.86.23.9574.
Abstract
In a previous paper, a model was presented showing how the group of Ca2+/calmodulin-dependent protein kinase II molecules contained within a postsynaptic density could stably store a graded synaptic weight. This paper completes the model by showing how bidirectional control of synaptic weight could be achieved. It is proposed that the quantitative level of the activity-dependent rise in postsynaptic Ca2+ determines whether the synaptic weight will increase or decrease. It is further proposed that reduction of synaptic weight is governed by protein phosphatase 1, an enzyme indirectly controlled by Ca2+ through reactions involving phosphatase inhibitor 1, cAMP-dependent protein kinase, calcineurin, and adenylate cyclase. Modeling of this biochemical system shows that it can function as an analog computer that can store a synaptic weight and modify it in accord with the Hebb and anti-Hebb learning rules.
摘要
在之前的一篇论文中，提出了一个模型，展示了包含在突触后致密物中的一组钙/钙调蛋白依赖性蛋白激酶II分子如何能够稳定地存储分级突触权重。本文通过展示如何实现突触权重的双向控制来完善该模型。有人提出，突触后钙的活性依赖性升高的定量水平决定了突触权重是增加还是减少。进一步提出，突触权重的降低由蛋白磷酸酶1控制，该酶通过涉及磷酸酶抑制剂1、环磷酸腺苷依赖性蛋白激酶、钙调神经磷酸酶和腺苷酸环化酶的反应由钙间接控制。对这个生化系统的建模表明，它可以作为一台模拟计算机，能够存储突触权重并根据赫布和反赫布学习规则对其进行修改。
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