A secondary working memory challenge preserves primary place strategies despite overtraining.

Learning by repetition engages distinct cognitive strategies whose contributions are adjusted with experience. Early in learning, performance relies upon flexible, attentive strategies. With extended practice, inflexible, automatic strategies emerge. This transition is thought fundamental to habit formation and applies to human and animal cognition. In the context of spatial navigation, place strategies are flexible, typically employed early in training, and rely on the spatial arrangement of landmarks to locate a goal. Response strategies are inflexible, become dominant after overtraining, and utilize fixed motor sequences. Although these strategies can operate independently, they have also been shown to interact. However, since previous work has focused on single-choice learning, if and how these strategies interact across sequential choices remains unclear. To test strategy interactions across sequential choices, we utilized various two-choice spatial navigation tasks administered on the Opposing Ts maze, an apparatus for rodents that permits experimental control over strategy recruitment. We found that when a second choice required spatial working memory, the transition to response navigation on the first choice was blocked. Control experiments specified this effect to the cognitive aspects of the secondary task. In addition, response navigation, once established on a single choice, was not reversed by subsequent introduction of a secondary choice reliant on spatial working memory. These results demonstrate that performance strategies interact across choices, highlighting the sensitivity of strategy use to the cognitive demands of subsequent actions, an influence from which overtrained rigid actions may be protected.

Removal of area CA3 from hippocampal slices induces postsynaptic plasticity at Schaffer collateral synapses that normalizes CA1 pyramidal cell discharge.

Neural networks that undergo acute insults display remarkable reorganization. This injury related plasticity is thought to permit recovery of function in the face of damage that cannot be reversed. Previously, an increase in the transmission strength at Schaffer collateral to CA1 pyramidal cell synapses was observed after long-term activity reduction in organotypic hippocampal slices. Here we report that, following acute preparation of adult rat hippocampal slices and surgical removal of area CA3, input to area CA1 was reduced and Schaffer collateral synapses underwent functional strengthening. This increase in synaptic strength was limited to Schaffer collateral inputs (no alteration to temporoammonic synapses) and acted to normalize postsynaptic discharge, supporting a homeostatic or compensatory response. Short-term plasticity was not altered, but an increase in immunohistochemical labeling of GluA1 subunits was observed in the stratum radiatum (but not stratum moleculare), suggesting increased numbers of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors and a postsynaptic locus of expression. Combined, these data support the idea that, in response to the reduction in presynaptic activity caused by removal of area CA3, Schaffer collateral synapses undergo a relatively rapid increase in functional efficacy likely supported by insertion of more AMPARs, which maintains postsynaptic excitability in CA1 pyramidal neurons. This novel fast compensatory plasticity exhibits properties that would allow it to maintain optimal network activity levels in the hippocampus, a brain structure lauded for its ongoing experience-dependent malleability.