Sensory reinforced corticostriatal plasticity

Background: Regional changes in corticostriatal transmission induced by phasic dopaminergic signals are an essential feature of the neural network responsible for instrumental reinforcement that occurs during action discovery. However, the timing of signals in early models of corticostriatal plasticity is difficult to reconcile with behavioral reinforcement learning where the reinforcer is normally delayed with respect to the selection and execution of causally-related actions.

Objective: While recent studies have started to address the relevance of delayed reinforcement signals and their impact on corticostriatal processing, our objective was to establish a model in which a sensory reinforcer triggers appropriately delayed reinforcement signals relayed to the striatum via intact neuronal pathways and to investigate the effects on corticostriatal plasticity.

Methods: We measured corticostriatal plasticity with electrophysiological recordings, a light flash as a natural sensory reinforcer, and pharmacological manipulations in an in vivo anaesthetized rat preparation.

Results: We demonstrate that the spiking of striatal neurons evoked by single pulse stimulation of motor cortex can be potentiated by a natural sensory reinforcer, operating through intact afferent pathways, with signal timing approximating that required for behavioral reinforcement. The observed potentiation of corticostriatal neurotransmission was attenuated by pharmacological blockade of dopamine receptors.

Conclusion: This novel in vivo model of corticostriatal plasticity offers a behaviorally relevant framework with which to address the physiological, anatomical, cellular and molecular bases of instrumental reinforcement learning.