FIGURE 5.

Schematic illustration of trauma-induced changes over time. Note that each panel represents one cortical recording patch with lateral corticocortical connections represented by the uppermost arrows (supragranular layer boundary, gray dashed lines), local intracolumnar connections in the granular layer boundaries, and corresponding thalamocortical inputs that arise via the infragranular layer boundaries. Acoustic trauma led to increased auditory thresholds, which we found to be present over the entire tonotopic gradient (cf. Figure 1C). On a columnar level, as indicated by the scheme, this can be explained by noise-trauma induced decreased strength of local thalamic input to ACx (indicated by dashed thin blue arrow in middle panel; cf. Figures 3A,D). While overall columnar activity was consistently decreased across the tonotopic gradient, the relative contribution of corticocortical activity was increased immediately after the trauma (upper red arrows in middle panel; cf. Figure 2). After recovery over weeks, these acute effects were reversed: while increased sensory input from thalamus was now coupled with an increased local intracolumnar gain of tone-evoked cortical activity (red arrows in right panel; cf. Figure 4), the recruitment of lateral corticocortical circuits was relatively decreased to pre-trauma condition levels or even below (for frequency regions above trauma, blue dashed arrow in right panel) (cf. Figure 2).