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Learning by imitation is fundamental to both communication and social behavior and requires the conversion of complex, nonlinear sensory codes for perception into similarly complex motor codes for generating action. To understand the neural substrates underlying this conversion, we study sensorimotor transformations in songbird cortical output neurons of a basal-ganglia pathway involved in song learning. Despite the complexity of sensory and motor codes, we find a simple, temporally specific, causal correspondence between them. Sensory neural responses to song playback mirror motor-related activity recorded during singing, with a temporal offset of roughly 40 ms, in agreement with short feedback loop delays estimated using electrical and auditory stimulation. Such matching of mirroring offsets and loop delays is consistent with a recent Hebbian theory of motor learning and suggests that cortico-basal ganglia pathways could support motor control via causal inverse models that can invert the rich correspondence between motor exploration and sensory feedback. [ABSTRACT FROM AUTHOR]

Across many studies, genetically modified animals with enhanced synaptic plasticity exhibit either enhanced or impaired learning, raising a fundamental conceptual puzzle: how can the enhancement of plasticity yield these opposite learning outcomes? Here we show that the recent history of experience can determine whether mice with enhanced plasticity exhibit enhanced or impaired learning in response to the same training. Mice with enhanced cerebellar LTD, due to double genetic knockout (DKO) of Class-I major histocompatibility molecules H2-Kb and H2-Db (KbDb-/-), exhibited oculomotor learning deficits. However, the same mice exhibited enhanced oculomotor learning after the appropriate pre-training. Theoretical analysis revealed that complex synapses with history-dependent learning rules could recapitulate our experimental results, and suggested that saturation may be a key factor limiting the ability of enhanced plasticity to support enhanced learning. Consistent with this, optogenetic stimulation designed to saturate cerebellar LTD produced the same, specific learning impairment in wildtype mice that was observed in DKO mice without such stimulation. Overall, our results suggest that the recent history of activity in a circuit and the threshold for synaptic plasticity conspire to effect divergent learning outcomes. [ABSTRACT FROM AUTHOR]