Anatomical evidence for cortical subdivisions based on vertically discrete thalamic projections from the ventral posterior nucleus to cortical barrels in the rat

The unit in monkey striate cortex, at least with respect to eye dominance, was a long slab-shaped column of cortex rather than the vertical cylinder originally proposed by Lorente de N6, however, one possible reason for this difference not discussed is that the 'eye preference column' may not be a unitary structure.

Abstract

Diffuse traumatic brain injury (TBI) induces damage to the neuro-vascular-glial units with the hallmark pathology as diffuse axonal injury (DAI) throughout the brain in concert with persisting neuroinflammatory responses and molecular cascades that disrupt global circuit function without gross focal lesions. In response to axonal injury, neuroplasticity works to compensate, repair, and reconnect damaged circuits. However, the nature of the axonal injury is the loss of short- and long-range projections adjacent to intact neurons, where maladaptive processes of surviving neurons result in novel or atypical reconnections that do not reconstitute the integrity of the original circuit. While extensive literature supports circuit reorganization after TBI, the full contribution to chronic behavioral morbidity and the time course of reorganization is yet to be investigated. Rehabilitation also plays an essential role in adaptive neuroplasticity—fundamental for functional recovery from TBI, yet the science behind optimal timing, type, intensity, and duration requires further investigation. Here, we discuss evidence in the literature that supports the theory of how diffuse TBI instigates and propagates progressive circuit reorganization that underlies behavioral morbidity. Due to the complex nuances of circuit function, we then propose advantages for employing the somatosensory whisker barrel circuit as a simplified behaviorally-relevant circuit and review work investigating the injury-induced circuit disruption and reorganization contributing to post-traumatic morbidity. Finally, we suggest that this circuit has exceptional potential to serve as an in vivo model of circuit disruption and reorganization for use with pharmacological intervention and for guiding the development of circuit-directed rehabilitation to recalibrate dysfunctional circuits and improve long-term outcomes.