Induction of Chimera States in Hindmarsh-Rose Neurons through Astrocytic Modulation: Implications for Learning Mechanisms

Abstract Chimera states, a form of partial synchronization in neural networks, are characterized by the coexistence of synchronized and asynchronous regions. These states are crucial for various cognitive functions, such as learning and information processing. Conversely, abnormal synchronization—often referred to as hyper-synchronization—can lead to pathological conditions such as epilepsy and Parkinson’s disease. Understanding the mechanisms underlying synchronization can provide valuable insights for developing effective therapeutic strategies for these disorders. Astrocyte, a primary type of glial cell, plays a pivotal role in modulating neural synchrony. They influence the synchronization threshold of neurons by providing feedback through the release of gliotransmitters, promoting group firing of neurons within the astrocyte’s domain. This research aims to explore how astrocytes can facilitate the conversion of hyper-synchronized states into healthy chimera states within neural networks. This process is vital for maintaining normal brain function and may be critical to advancing treatments for neurological conditions. We analyzed how astrocytes can induce chimera states in nonlocally two-dimensional Hindmarsh-Rose neurons, which serve as realistic models of neuronal ensembles. Our findings demonstrate that astrocytes can effectively transition unhealthy hyper-synchronization states into healthy chimera states. Furthermore, by analyzing time spans, spatiotemporal patterns, inter-spike interval distributions (ISI), and phase plane diagrams of 2D H-R neurons, we validated our hypothesis about the crucial role of astrocytes in the development of chimera states. The outcomes may pave the way for innovative therapeutic approaches to restore normal neural activity patterns, ultimately improving patient outcomes in conditions such as epilepsy and Parkinson’s disease. Competing Interest Statement The authors have declared no competing interest.