New cells are generated throughout life and integrate into the hippocampus via the process of adult neurogenesis. Epileptogenic brain injury induces many structural changes in the hippocampus, including the death of interneurons and altered connectiv
ity patterns. The pathological neurogenic niche is associated with aberrant neurogenesis, though the role of the network-level changes in development of epilepsy is not well understood. In this paper, we use computational simulations to investigate the effect of network environment on structural and functional outcomes of neurogenesis. We find that small-world networks with external stimulus are able to be augmented by activity-seeking neurons in a manner that enhances activity at the stimulated sites without altering the network as a whole. However, when inhibition is decreased or connectivity patterns are changed, new cells are both less responsive to stimulus and the new cells are more likely to drive the network into bursting dynamics. Our results suggest that network-level changes caused by epileptogenic injury can create an environment where neurogenic reorganization can induce or intensify epileptic dynamics and abnormal integration of new cells.
We investigate clustering of malignant glioma cells. emph{In vitro} experiments in collagen gels identified a cell line that formed clusters in a region of low cell density, whereas a very similar cell line (which lacks an important mutation) did not
cluster significantly. We hypothesize that the mutation affects the strength of cell-cell adhesion. We investigate this effect in a new experiment, which follows the clustering dynamics of glioma cells on a surface. We interpret our results in terms of a stochastic model and identify two mechanisms of clustering. First, there is a critical value of the strength of adhesion; above the threshold, large clusters grow from a homogeneous suspension of cells; below it, the system remains homogeneous, similarly to the ordinary phase separation. Second, when cells form a cluster, we have evidence that they increase their proliferation rate. We have successfully reproduced the experimental findings and found that both mechanisms are crucial for cluster formation and growth.
We study a generalization of the voter model on complex networks, focusing on the scaling of mean exit time. Previous work has defined the voter model in terms of an initially chosen node and a randomly chosen neighbor, which makes it difficult to di
sentangle the effects of the stochastic process itself relative to the network structure. We introduce a process with two steps, one that selects a pair of interacting nodes and one that determines the direction of interaction as a function of the degrees of the two nodes and a parameter $alpha$ which sets the likelihood of the higher degree node giving its state. Traditional voter model behavior can be recovered within the model. We find that on a complete bipartite network, the traditional voter model is the fastest process. On a random network with power law degree distribution, we observe two regimes. For modest values of $alpha$, exit time is dominated by diffusive drift of the system state, but as the high nodes become more influential, the exit time becomes becomes dominated by frustration effects. For certain selection processes, a short intermediate regime occurs where exit occurs after exponential mixing.
