Authors: Matthijs Kusters¹, Spencer Olson¹’², Mario Senden¹, Michelle Moerel¹’³
¹Dept. of Cognitive Neuroscience, FPN, Maastricht University; ²ExpORL, Dept. Neuroscience, KU Leuven; ³MaCSBio, FSE, Maastricht University
Background: Human hearing is remarkably flexible. In crowded environments, we effortlessly attend to relevant sounds while ignoring irrelevant ones. The circuitry between the auditory thalamus (MGB), primary auditory cortex (PAC), and thalamic reticular nucleus (TRN) has been proposed as key for attentive sound processing. Whether this circuitry can support the computations underlying selective attention remains unknown.
Method: The Wilson-Cowan Cortical Model was adapted to include MGB-PAC-TRN circuitry, with each region represented by inhibitory-excitatory neuron populations (except the TRN, which contains only inhibitory populations). Optimization proceeded in three steps: (1) a sensitivity analysis across 40,000 simulations; (2) model selection based on biological plausibility of firing rates; and (3) parameter tuning to match electrophysiological literature. Robustness was evaluated by monitoring parameter changes on firing rates and tuning.
Results: From 40,000 simulations, 2,710 viable parameter sets were identified and narrowed to a single optimal configuration. The final model produced firing rates and tuning widths consistent with electrophysiological literature, with MGB and PAC exhibiting sharp frequency tuning and TRN showing broader tuning approximately 2.5 times that of MGB. Multiple parameter configurations yielded plausible responses, indicating the model is not constrained to a unique solution.
Conclusion: The implemented MGB-PAC-TRN circuitry demonstrates that the proposed corticothalamic network can be incorporated into a computationally stable model with biologically plausible dynamics. Future work should implement attentional modulation to assess whether this circuitry reproduces neural dynamics observed during selective attention tasks. The model also holds potential for tinnitus research, where TRN dysfunction is hypothesized to allow aberrant signals to propagate into the auditory cortex.
