#PaperOfTheDay, "A Simple Rule for Dendritic Spine and Axonal Bouton Formation Can Account for Cortical Reorganization after Focal Retinal Lesions" by Butz et al (2013).

It deals with #StructuralPlasticity in the #brain, the ability of cells (here #neurons) to reorganize their connections to maintain their activity in a given range.

Authors model how the brain can recover from a lesion that cuts some neurons from their normal sensory input.

https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003259

#science #neuroscience

A Simple Rule for Dendritic Spine and Axonal Bouton Formation Can Account for Cortical Reorganization after Focal Retinal Lesions

Author Summary The adult brain is less hard-wired than traditionally thought. About ten percent of synapses in the mature visual cortex is continually replaced by new ones (structural plasticity). This percentage greatly increases after lasting changes in visual input. Due to the topographically organized nerve connections from the retina in the eye to the primary visual cortex in the brain, a small circumscribed lesion in the retina leads to a defined area in the cortex that is deprived of input. Recent experimental studies have revealed that axonal sprouting and dendritic spine turnover are massively increased in and around the cortical area that is deprived of input. However, the driving forces for this structural plasticity remain unclear. Using a novel computational model, we examine whether the need for activity homeostasis of individual neurons may drive cortical reorganization after lasting changes in input activity. We show that homeostatic growth rules indeed give rise to structural and functional reorganization of neuronal networks similar to the cortical reorganization observed experimentally. Understanding the principles of structural plasticity may eventually lead to novel treatment strategies for stimulating functional reorganization after brain damage and neurodegeneration.

The theoretical model they use (MSP) was seminal in the field, it provides a simple way to assess how connectivity may depend on changes in neuronal activity.
The root of the model is a simple 1D dynamical system with one fixed point: neurons create connections if they are less active than they should, they delete them if they are too active.
With this simple model, they show that, for some parameters, they can reproduce qualitatively some properties of the healing behavior in the visual system.

Although this model is very interesting, it is quite simple and leave much room for further research.
The influence of inhibitory neurons, for instance, is under-studied and their growth rule in the original model destabilizes the network.
Despite a recent preprint by Sinha et al 2020 that extends the model in an interesting way and tries to tackle some of its shortcomings, I believe there is still much to explore on structural plasticity modeling.

https://www.biorxiv.org/content/10.1101/810846v2.full