A model of human motor sequence learning explains facilitation and interference effects based on spike-timing dependent plasticity

• Published in: PLoS computational biology Vol. 13; no. 8; p. e1005632
• Main Authors: Wang, Quan, Rothkopf, Constantin A., Triesch, Jochen
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01.08.2017; Public Library of Science (PLoS)
• Subjects: Action Potentials - physiology; Behavior; Biology and Life Sciences; Brain; Computational Biology; Computer and Information Sciences; Driving ability; Experiments; Firing pattern; Homeostatic plasticity; Human performance; Human subjects; Humans; Interference; IP (Internet Protocol); Learning; Learning - physiology; Memory; Models, Neurological; Motor skill learning; Motor skills; Neural circuitry; Neural networks; Neuronal Plasticity - physiology; Neurons; Neuroplasticity; Neurosciences; Physiological aspects; Plasticity (neural); Recurrent neural networks; Social Sciences; Studies; Synaptic plasticity; Training; Germany
• ISSN: 1553-7358; 1553-734X; 1553-7358
• DOI: 10.1371/journal.pcbi.1005632

The ability to learn sequential behaviors is a fundamental property of our brains. Yet a long stream of studies including recent experiments investigating motor sequence learning in adult human subjects have produced a number of puzzling and seemingly contradictory results. In particular, when subjects have to learn multiple action sequences, learning is sometimes impaired by proactive and retroactive interference effects. In other situations, however, learning is accelerated as reflected in facilitation and transfer effects. At present it is unclear what the underlying neural mechanism are that give rise to these diverse findings. Here we show that a recently developed recurrent neural network model readily reproduces this diverse set of findings. The self-organizing recurrent neural network (SORN) model is a network of recurrently connected threshold units that combines a simplified form of spike-timing dependent plasticity (STDP) with homeostatic plasticity mechanisms ensuring network stability, namely intrinsic plasticity (IP) and synaptic normalization (SN). When trained on sequence learning tasks modeled after recent experiments we find that it reproduces the full range of interference, facilitation, and transfer effects. We show how these effects are rooted in the network's changing internal representation of the different sequences across learning and how they depend on an interaction of training schedule and task similarity. Furthermore, since learning in the model is based on fundamental neuronal plasticity mechanisms, the model reveals how these plasticity mechanisms are ultimately responsible for the network's sequence learning abilities. In particular, we find that all three plasticity mechanisms are essential for the network to learn effective internal models of the different training sequences. This ability to form effective internal models is also the basis for the observed interference and facilitation effects. This suggests that STDP, IP, and SN may be the driving forces behind our ability to learn complex action sequences.