Associative memory performance in peripherally-lesioned networks repaired by homeostatic structural plasticity

In spite of a plethora of peripheral lesion experiments documenting that structural plasticity causes large scale changes in brain networks, our understanding of the mechanisms of structural plasticity remains limited. Structural plasticity acts over extended periods of time, albeit at a slow rate, to modify network connectivity by the formation and removal of synapses. Alterations in network connectivity are expected to affect network function, but the resulting functional consequences of structural plasticity have not been studied in detail.

To study the activity dependent growth characteristics of neurites, which underlie network reconfiguration, we previously developed a novel model of peripheral lesioning and subsequent repair in a balanced cortical Asynchronous Irregular (AI) spiking network [6]. The network used in our model, which represents a physiological brain network, was selected since it has been demonstrated to function as an attractor-less associative memory store [5]. Using this new model, we investigated the functional effects of repair mediated by homeostatic structural plasticity on the network. We stored associative memories in the network and recalled them at different stages of the simulation by stimulating a random subset of their neurons: before deafferentation, after deafferentation but before repair, and after deafferentation during repair. At each recall, recall performance was quantified using a Signal to Noise ratio (SNR) metric.

Associative memories that include neurons deafferented by the peripheral lesion experience a reduction in their recall performance proportionate to the number of deprived neurons. Our results indicate that while structural plasticity restores activity of deafferented neurons to pre-injury levels, it does not restore the performance of the stored associative memories. This suggests that associative memories stored before a peripheral lesion are not necessarily protected in the repair process. Further research is needed to explore whether the repair process can be modulated to retain the performance of the stored associative memories.