Towards neuro-inspired symbolic models of cognition: linking neural dynamics to behaviors through asynchronous communications

A computational architecture modeling the relation between perception and action is proposed. Basic brain processes representing synaptic plasticity are first abstracted through asynchronous communication protocols and implemented as virtual microcircuits. These are used in turn to build mesoscale circuits embodying parallel cognitive processes. Encoding these circuits into symbolic expressions gives finally rise to neuro-inspired programs that are compiled into pseudo-code to be interpreted by a virtual machine. Quantitative evaluation measures are given by the modification of synapse weights over time. This approach is illustrated by models of simple forms of behaviors exhibiting cognition up to the third level of animal awareness. As a potential benefit, symbolic models of emergent psychological mechanisms could lead to the discovery of the learning processes involved in the development of cognition. The executable specifications of an experimental platform allowing for the reproduction of simulated experiments are given in “Appendix”

Implications of Tn5-associated adjacent deletions.

The prokaryotic transposable element Tn5 has been found to promote the formation of adjacent deletions. The frequency of adjacent deletion formation is much lower than that of normal transposition events. Like normal transposition, however, adjacent deletion formation requires the activity of the transposase protein. The deletions can be divided into two classes, as distinguished by their endpoints. The occurrence of one of the two deletion classes is increased when the frequency of normal transposition is reduced by the introduction of a deletion or a certain base substitution at one of the two outside ends (OEs). The nature of the base substitution at the mutant OE influences the class of deletion found adjacent to the wild-type OE, even though these two ends are about 12 kbp apart. By studying the formation of these deletions, we have gained some insight into the way in which the transposase interacts with the OEs. Our observations suggest that there is a protein-mediated interaction between the two ends, that different end base pairs are involved in different transposition-related processes, and that the adjacent deletions are the result of nonproductive attempts at transposition