神经集合通过局部学习机制实现因果方向识别,无需反向传播。
Causal Learning with Neural Assemblies

- 利用神经集合的投影、局部可塑性和稀疏胜者选择实现方向性学习。
- 在已知结构下达到完美结构恢复,权重差异与信号传播重合度高。
- 结果可追溯到具体神经元和突触不对称性,适合可解释因果建模研究。
神经集合——通过共同激活而强化的神经元群组——能否学习变量间的因果方向?尽管已被证实是分类、解析和规划的通用计算基础,但其对因果方向性的内化尚未得到验证。本文证明,神经集合固有的操作——投影、局部可塑性控制和稀疏胜者选择——足以实现方向性学习。我们提出DIRECT(DIRectional Edge Coupling/Training)机制,通过自适应增益调度协同激活源与目标集合,以建立有向关系。不同于依赖反向传播的方法,DIRECT仅依赖局部可塑性,使因果推断可在机制层面被审计。通过双读出验证策略:(i) 突触强度不对称性,衡量正向与反向连接间的权重差距;(ii) 功能传播重叠度,量化方向性信号流的可靠性。在多个领域中,该框架在监督已知结构设定下实现了完美结构恢复。研究确立了神经集合作为生物合理动力学与形式因果模型之间的可审计桥梁,提供一种‘设计即可解释’的框架,其中因果主张可追溯至特定神经元胜者与突触不对称性。
原文摘要 · Abstract (English)
Can Neural Assemblies -- groups of neurons that fire together and strengthen through co-activation -- learn the direction of causal influence between variables? While established as a computationally general substrate for classification, parsing, and planning, neural assemblies have not yet been shown to internalize causal directionality. We demonstrate that the inherent operations of neural assemblies -- projection, local plasticity control, and sparse winner selection -- are sufficient for directional learning. We introduce DIRECT (DIRectional Edge Coupling/Training), a mechanism that co-activates source and target assemblies under an adaptive gain schedule to internalize directed relations. Unlike backpropagation-based methods, DIRECT relies solely on local plasticity, making the resulting causal claims auditable at the mechanism level. Our findings are verified through a dual-readout validation strategy: (i) synaptic-strength asymmetry, measuring the emergent weight gap between forward and reverse links, and (ii) functional propagation overlap, quantifying the reliability of directional signal flow. Across multiple domains, the framework achieves perfect structural recovery under a supervised, known-structure setting. These results establish neural assemblies as an auditable bridge between biologically plausible dynamics and formal causal models, offering an "explainable by design" framework where causal claims are traceable to specific neural winners and synaptic asymmetries.
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