Fig. 3.

Competing models of the Thalamocortical circuit as described by factors 1 and 2 (9 architectures times 16 modulatory configurations). The diagram on the top (factor 1: architecture) describes the 9 families of models constructed to elucidate which thalamocortical projections are the most plausible explanation for the generation of beta oscillations (1.- 3.) accounts for a singular projection from thalamus to motor cortex via superficial pyramidal cells, middle pyramidal cells and deep pyramidal cells; (4.- 6.) accounts for two afferents to two excitatory subpopulations of the motor cortex via superficial and middle pyramidal cells, middle and deep pyramidal cells and superficial plus deep pyramidal cells, and (7.- 9.) accounts for projections to the superficial pyramidal subpopulation and inhibitory interneurons, the middle pyramidal subpopulation and inhibitory interneurons and deep pyramidal cells and inhibitory interneurons. To disclose the synaptic modulation (intrinsic and/or extrinsic) responsible for an enhancement of beta power, the models on the bottom (factor 2: modulatory configuration) feature 16 different modulatory configurations, under each of the 9 architectures described above. The first eight set of connections (1.-8.) entail extrinsic and intrinsic synaptic modulation (except for model 8, with no intrinsic modulation) and the second eight set of connections (9.-16.) considers intrinsic modulation only. The intrinsic modulatory connections in family 2 were: (1. and 9.) cortical modulation via reciprocal connection between superficial and deep pyramidal subpopulations; (2. and 10.) cortical modulation via reciprocal connection between superficial and middle pyramidal subpopulations; (3. and 11.) cortical modulation via self-inhibitory connection of the inhibitory interneurons subpopulation; (4. and 12.) thalamic modulation via reciprocal connection between reticular cells and relay cells; (5. and 13.) cortical and thalamic modulation via reciprocal connection between superficial and deep pyramidal subpopulations plus reciprocal connection between reticular cells and relay cells; (6. and 14.) cortical modulation via reciprocal connection between superficial and middle pyramidal subpopulations plus reciprocal connection between reticular cells and relay cells; (7. and 8.) self-inhibitory connection of the inhibitory interneuron subpopulation plus reciprocal connection between reticular cells and relay cells and lastly, (8. and 16.) the null hypothesis that neither extrinsic nor intrinsic connections change to explain condition specific changes in cortical beta power (i.e. enhancement of beta).