Network Supervision of Adult Experience and Learning Dependent Sensory Cortical Plasticity
The brain is capable of remodeling throughout life. The sensory cortices provide a useful preparation for studying neuroplasticity both during development and thereafter. In adulthood, sensory cortices change in the cortical area activated by behaviorally relevant stimuli, by the strength of response within that activated area, and by the temporal profiles of those responses. Evidence supports forms of unsupervised, reinforcement, and fully supervised network learning rules. Studies on
... Studies on experience-dependent plasticity have mostly not controlled for learning, and they find support for unsupervised learning mechanisms. Changes occur with greatest ease in neurons containing α-CamKII, which are pyramidal neurons in layers II/III and layers V/VI. These changes use synaptic mechanisms including long term depression. Synaptic strengthening at NMDA-containing synapses does occur, but its weak association with activity suggests other factors also initiate changes. Studies that control learning find support of reinforcement learning rules and limited evidence of other forms of supervised learning. Behaviorally associating a stimulus with reinforcement leads to a strengthening of cortical response strength and enlarging of response area with poor selectivity. Associating a stimulus with omission of reinforcement leads to a selective weakening of responses. In some preparations in which these associations are not as clearly made, neurons with the most informative discharges are relatively stronger after training. Studies analyzing the temporal profile of responses associated with omission of reward, or of plasticity in studies with different discriminanda but statistically matched stimuli, support the existence of limited supervised network learning. Major teaching points r Primary sensory cortex is plastic, or can change, throughout life. r The change is strongly influenced by behaviors in which the animal associates a stimulus with reinforcement or omission of reinforcement. r Association with reinforcement leads to a poorly selective increased responsiveness. r Association with omission of reward leads to a selective response suppression. r The neural mechanisms underlying increased responsiveness are poorly described and are not well explained solely by known synaptic plasticity mechanisms. r The neural mechanisms underlying response suppression appear to be well explained by synaptic long term depression. r Changes appear greatest in principal neurons in layers II/III and V/VI. r The changes are influenced by the neuromodulator acetylcholine. r Evidence supports that more central sensory cortices guide the response suppression seen when a stimulus is associated with omission of reward.