A MECHANISM FOR THE HEBB AND THE ANTI-HEBB PROCESSES UNDERLYING LEARNING AND MEMORY
A MECHANISM FOR THE HEBB AND THE ANTI-HEBB PROCESSES UNDERLYING LEARNING AND MEMORY
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DOI：
10.1073/pnas.86.23.9574
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发表时间：
1989-12-01
影响因子：
11.1
通讯作者：
LISMAN, J
中科院分区：
文献类型：
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作者：
LISMAN, J
在之前的一篇论文中，提出了一个模型，显示了突触后密度中包含的Ca2+/钙调素依赖性蛋白激酶II分子如何稳定地存储分级突触重量。本文通过展示如何实现突触重量的双向控制来完成该模型。我们认为，突触后Ca2+的活性依赖性上升的定量水平决定了突触重量的增加或减少。进一步提出，突触重量的减少是由蛋白磷酸酶1控制的，这种酶通过涉及磷酸酶抑制剂1、camp依赖性蛋白激酶、钙调磷酸酶和腺苷酸环化酶的反应间接受Ca2+控制。对该生化系统的建模表明，它可以像模拟计算机一样存储突触权重，并根据Hebb和anti-Hebb学习规则对其进行修改。
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.