Norepinephrine potentiates and serotonin depresses visual cortical responses by transforming eligibility traces

• DOI: 10.1038/s41467-022-30827-1
• Publication Date: 2022-06-09T10:03:35Z
• Authors: Su Z. Hong; Lukas Mesik; Cooper D. Grossman; Jeremiah Y. Cohen; Boram Lee; Daniel Severin; Hey-Kyoung Lee; Johannes W. Hell; Alfredo Kirkwood
• Keywords: 0301 basic medicine; 570; Serotonin; Neuronal Plasticity; Biomedical and Clinical Sciences; Science; Q; Long-Term Potentiation; Neurosciences; 610; Basic Behavioral and Social Science; Article; Machine Learning; Mice; Norepinephrine; 03 medical and health sciences; Mental Health; Information and Computing Sciences; Behavioral and Social Science; Synapses; Animals; Eye Disease and Disorders of Vision; Visual Cortex

AbstractReinforcement allows organisms to learn which stimuli predict subsequent biological relevance. Hebbian mechanisms of synaptic plasticity are insufficient to account for reinforced learning because neuromodulators signaling biological relevance are delayed with respect to the neural activity associated with the stimulus. A theoretical solution is the concept of eligibility traces (eTraces), silent synaptic processes elicited by activity which upon arrival of a neuromodulator are converted into a lasting change in synaptic strength. Previously we demonstrated in visual cortical slices the Hebbian induction of eTraces and their conversion into LTP and LTD by the retroactive action of norepinephrine and serotonin Here we show in vivo in mouse V1 that the induction of eTraces and their conversion to LTP/D by norepinephrine and serotonin respectively potentiates and depresses visual responses. We also show that the integrity of this process is crucial for ocular dominance plasticity, a canonical model of experience-dependent plasticity.