Miles R, Wong R K
Department of Neurology, Columbia University, New York, New York 10032.
Nature. 1987;329(6141):724-6. doi: 10.1038/329724a0.
Synaptic plasticity may result from changes at existing synapses or from alterations in the number of functional synaptic connections. In the hippocampus excitatory synaptic strength is persistently enhanced after tetanic stimulation. Here we report that latent synaptic pathways may also become functional. Simultaneous intracellular recordings were made from pairs of CA3 pyramidal cells in slices from guinea pig hippocampus. After stimulating afferent fibres repetitively, polysynaptic excitatory pathways between previously unconnected cells became apparent. The efficacy of recurrent inhibitory circuits was also reduced. The loss of inhibitory control is of interest because latent excitatory pathways are revealed after pharmacological suppression of inhibition. This plasticity in local synaptic circuits leads to the emergence of synchronous firing in groups of CA3 cells. The formation of groups of associated cells and the ability of some cells to initiate synchronous firing in a larger cell group through recurrent pathways is reminiscent of several models of information storage and recall in the cortex.
突触可塑性可能源于现有突触的变化或功能性突触连接数量的改变。在海马体中，强直刺激后兴奋性突触强度会持续增强。在此我们报告，潜在的突触通路也可能变得具有功能性。我们从豚鼠海马体切片中的成对CA3锥体细胞进行了同步细胞内记录。在反复刺激传入纤维后，先前未连接的细胞之间的多突触兴奋性通路变得明显。回返抑制回路的效能也降低了。抑制控制的丧失之所以令人关注，是因为在药理学抑制抑制作用后会揭示出潜在的兴奋性通路。局部突触回路中的这种可塑性导致CA3细胞群中同步放电的出现。相关细胞群的形成以及一些细胞通过回返通路在更大的细胞群中引发同步放电的能力让人联想到皮层中几种信息存储和回忆的模型。
