Dynamic Routing on a Static Structure: Noradrenergic Gatingof Cortical Wave Propagation

Stimulus-evoked cortical responses range from tightly localized activations to spatially extended traveling waves, yet the mechanisms through which these distinct regimes are flexibly recruited remain unclear. Based on neuroanatomical and neuroimaging evidence, we hypothesize that the noradrenergic (NA) arousal system, originating in the locus coeruleus (LC), dynamically modulates cortical gain to shape spatiotemporal propagation under a fixed anatomical backbone. To test this hypothesis, we extend an empirically grounded corticothalamic neural field model to incorporate an LC which delivers modulatory (gain-changing) rather than driving inputs to cortex. We then examine evoked responses under phasic versus tonic NA modulation, with geometry given by distance-dependent connectivity plus additional long-range fast-conducting non-local projections (FNPs). Phasic LC activation produces spatiotemporally sustained traveling waves of cortical activity, whereas tonic activation yields temporally prolonged but spatially localized responses; without modulation, waves are weak and dissipative. Timing and spatial pattern of LC engagement gate wave-onset latency and impose anisotropy, restricting propagation to modulated territories and halting it across unmodulated gaps. In the presence of long-range FNPs, modulation enables rapid non-local activation of distant cortical regions and sharply lowers the gain required for long-distance routing. These results identify NA phasic gain control as a parsimonious mechanism for variability in evoked dynamics and for context-dependent privileging of specific communication pathways over a largely static connectome. Author summaryThe brain doesnt always react to a stimulus in the same way: sometimes the response is local, while at other times it sweeps across the cortex as a wave. We propose that this flexibility can be controlled by the noradrenergic arousal signaling from the locus coeruleus (LC), which adjusts the gain of cortical circuits rather than directly driving them. Using an empirically grounded corticothalamic model augmented with an LC, we contrasted brief phasic bursts versus sustained tonic modulation. Phasic LC activity promoted robust traveling waves, while tonic activity produced longer-lasting but spatially confined responses. By further specifying when and where it engages, the LC can gate where waves start, which directions they travel, and where they stop--even across unmodulated gaps. When long-range connections are present, LC modulation also enables rapid, selective activation of distant targets and dramatically lowers the gain needed for long-distance routing. This neuromodulatory mechanism offers a simple, testable account of trial-to-trial variability in evoked dynamics, capturing a mechanism through which the brain can transiently privilege specific communication pathways through a static structural connectome.