Parkinson’s disease (PD) is a network disorder. Development of abnormally exaggerated beta band activity in the parkinsonian brain has been linked with motor symptoms. However, the cellular and circuit mechanisms underlying the generation of this abnormal beta activity remain undefined. Our research focus has lately turned to consideration of PD pathology in motor cortex (M1) cells and synapses. M1 is the final common pathway from telencephalon to brainstem and spinal cord, and will therefore play a disproportionate role in dysfunction for execution of fine-motor tasks. Using M1 slice electrophysiology, we have shown a 64% reduction in response of corticospinal pyramidal-tract-type neurons (PTs) to somatic current clamp in 6-OHDA-lesioned, parkinsonian, mice. Computer modeling (NEURON simulator. detailed >10k multicompartment network model) showed that this 64% decrease in PT excitability resulted in a paradoxical 25% increase in PT network firing rate due to the complexities of feedback and feedforward excitatory and inhibitory loops through parvalbumin interneurons and intratelencephalic (IT) neurons. A concomitant network change was a 2.2-fold strengthening of beta strength in LFP with slowing from 19 to 14 Hz; with duty cycle (peak duration/period) decreasing from 46% to 36%, and synchronous PT firing increasing 2.6-fold. We suggest that these changes could contribute to the beta oscillation alterations that have been observed in PD. Figure shows control (left) vs parkinsonian (right) A LFP, raster, PT spike histogram, B select PT voltage traces out of ~1k, C rate comparisons.