Linster Christiane, Maloney Michaella, Patil Madhvi, Hasselmo Michael E
Department of Psychology Center for Memory and Brain and Program in Neuroscience, Boston University, 2 Cummington Street, Boston, MA 02215, USA.
Neurobiol Learn Mem. 2003 Nov;80(3):302-14. doi: 10.1016/s1074-7427(03)00078-9.
Computational modeling assists in analyzing the specific functional role of the cellular effects of acetylcholine within cortical structures. In particular, acetylcholine may regulate the dynamics of encoding and retrieval of information by regulating the magnitude of synaptic transmission at excitatory recurrent connections. Many abstract models of associative memory function ignore the influence of changes in synaptic strength during the storage process and apply the effect of these changes only during a so-called recall-phase. Efforts to ensure stable activity with more realistic, continuous updating of the synaptic strength during the storage process have shown that the memory capacity of a realistic cortical network can be greatly enhanced if cholinergic modulation blocks transmission at synaptic connections of the association fibers during the learning process. We here present experimental data from an olfactory cortex brain slice preparation showing that previously potentiated fibers show significantly greater suppression (presynaptic inhibition) by the cholinergic agonist carbachol than unpotentiated fibers. We conclude that low suppression of non-potentiated fibers during the learning process ensures the formation of self-organized representations in the neural network while the higher suppression of previously potentiated fibers minimizes interference between overlapping patterns. We show in a computational model of olfactory cortex, that, together, these two phenomena reduce the overlap between patterns that are stored within the same neural network structure. These results further demonstrate the contribution of acetylcholine to mechanisms of cortical plasticity. The results are consistent with the extensive evidence supporting a role for acetylcholine in encoding of new memories and enhancement of response to salient sensory stimuli.
计算模型有助于分析乙酰胆碱在皮质结构中的细胞效应的特定功能作用。特别是,乙酰胆碱可能通过调节兴奋性递归连接处突触传递的幅度来调节信息编码和检索的动态过程。许多联想记忆功能的抽象模型忽略了存储过程中突触强度变化的影响,仅在所谓的回忆阶段应用这些变化的效果。在存储过程中通过更现实、持续更新突触强度来确保稳定活动的努力表明,如果胆碱能调制在学习过程中阻断联合纤维突触连接处的传递,那么现实皮质网络的记忆容量可以大大提高。我们在此展示了来自嗅皮质脑片制备的实验数据,表明先前增强的纤维比未增强的纤维对胆碱能激动剂卡巴胆碱表现出明显更大的抑制(突触前抑制)。我们得出结论,学习过程中对未增强纤维的低抑制确保了神经网络中自组织表征的形成,而对先前增强纤维的更高抑制则最大限度地减少了重叠模式之间的干扰。我们在嗅皮质的计算模型中表明,这两种现象共同减少了存储在同一神经网络结构内的模式之间的重叠。这些结果进一步证明了乙酰胆碱对皮质可塑性机制的贡献。这些结果与支持乙酰胆碱在新记忆编码和对显著感觉刺激反应增强中起作用的大量证据一致。