• basal ganglia
• beta oscillations
• computational model
• gamma oscillations
• neuroscience
• Parkinson's disease

The basal ganglia are a group of nuclei in the central nervous system that play a crucial role in motor control, behaviour, learning, and emotions. This thesis presents a computational model comprising over 15,000 spiking neurons across six populations to explore the mechanisms driving gamma oscillations (i.e., neural oscillations above 30 Hz) observed experimentally in these structures.
Analyses of the power spectral densities of neuronal activity generated by the model reveal that both the prototypic populations of the globus pallidus and the D2 medium spiny neurons exhibit gamma oscillations, approximately at 140 Hz and 70 Hz, respectively. The disconnection of self-inhibition within these nuclei demonstrates that such projections are essential for generating these rhythms. Additionally, the oscillation frequency is strongly modulated by excitatory inputs and the synaptic properties of these self-inhibitory connections.
The model also shows a significant interaction between gamma oscillations and pathological beta oscillations (10–30 Hz), with the phase of beta rhythms modulating both the amplitude and frequency of gamma oscillations. Notably, D2 gamma oscillations would not be present without the modulation induced by the beta rhythms.
In conclusion, this thesis successfully identifies potential sources of gamma oscillations in the basal ganglia and highlights the importance of understanding their interaction with beta oscillations. These insights are crucial for advancing our understanding of both the physiology and pathology of the basal ganglia. Furthermore, this work provides a novel perspective that could inform new translational approaches to existing treatments for Parkinson's disease, including both open-loop and closed-loop deep brain stimulation.