Abstract
Grid cells (GCs) in the medial entorhinal cortex (mEC) have the property of having their firing activity spatially tuned to a regular triangular lattice. Several theoretical models for grid field formation have been proposed, but most assume that place cells (PCs) are a product of the grid cell system. There is, however, an alternative possibility that is supported by various strands of experimental data. Here we present a novel model for the emergence of gridlike firing patterns that stands on two key hypotheses: (1) spatial information in GCs is provided from PC activity and (2) grid fields result from a combined synaptic plasticity mechanism involving inhibitory and excitatory neurons mediating the connections between PCs and GCs. Depending on the spatial location, each PC can contribute with excitatory or inhibitory inputs to GC activity. The nature and magnitude of the PC input is a function of the distance to the place field center, which is inferred from rate decoding. A biologically plausible learning rule drives the evolution of the connection strengths from PCs to a GC. In this model, PCs compete for GC activation, and the plasticity rule favors efficient packing of the space representation. This leads to gridlike firing patterns. In a new environment, GCs continuously recruit new PCs to cover the entire space. The model described here makes important predictions and can represent the feedforward connections from hippocampus CA1 to deeper mEC layers.

Abstract
Motivation: Ebola virus causes high mortality hemorrhagic fevers, with more than 25 000 cases and 10 000 deaths in the current outbreak. Only experimental therapies are available, thus, novel diagnosis tools and druggable targets are needed. Results: Analysis of Ebola virus genomes from the current outbreak reveals the presence of short DNA sequences that appear nowhere in the human genome. We identify the shortest such sequences with lengths between 12 and 14. Only three absent sequences of length 12 exist and they consistently appear at the same location on two of the Ebola virus proteins, in all Ebola virus genomes, but nowhere in the human genome. The alignment-free method used is able to identify pathogen-specific signatures for quick and precise action against infectious agents, of which the current Ebola virus outbreak provides a compelling example.