This manuscript distil theoretical approaches to emergence into a practical framework for assessing system behaviour focussed on “novelty” as a necessary condition for emergence and identifies a range of ways in which novelty can arise.
Abstract
The concept of emergence is key to understanding much of neurophysiology, neurodevelopment, and neurodegeneration. Many brain functions are underpinned by behaviour that emerges from interactions of components such as neurons, synapses, and glia. Perturbations such as ion channel mutations or trauma can lead to new types of, often detrimental, emergent behaviour. Typical approaches to neuroscience involve studying neural behaviour in a range of in vitro, in vivo, and in silico models designed to capture the key components of the brain region under investigation. Translating from these models back to the brain requires that the component interactions within the models can be mapped onto interactions in the brain. However, in many cases, this may not hold, leading to emergent behaviour that is not derivable from knowledge of the brain components in relative isolation. We thus need a framework that respects the prospective system-dependent differences in interactions. In this manuscript, we distil theoretical approaches to emergence into a practical framework for assessing system behaviour focussed on “novelty” as a necessary condition for emergence and identify a range of ways in which novelty can arise. We consider how different approaches for investigating system behaviour can be applied in different contexts and when these might fail. We provide examples of different forms of novelty in neuroscience contexts and then apply the framework to understanding the specific case of epilepsy. We end by outlining a set of guiding principles for designing experiments and models for understanding emergent behaviour in neural systems.
Broadly speaking, neuroplasticity can be defined as the nervous system’s ability to adapt as a response to intrinsic or extrinsic stimuli by reorganising its structure, functions, or connections. Once a highly debated concept in neuroscience, neuroplasticity is now recognised as a fundamental mechanism by which the human brain adapts, learns, and recovers throughout our lives. This paper examines the cellular and structural processes that allow the brain to reorganise its neural pathways in response to internal and external stimuli. It also highlights the critical role of neuroplasticity in lifelong learning, memory formation, and functional recovery following traumatic brain injuries or strokes. Furthermore, the clinical implications of self-directed neuroplasticity are explored, demonstrating how intentional behavioural changes can aid in the treatment of mental health disorders like depression and anxiety. Ultimately, understanding neuroplasticity shifts the standard of the human brain from a static organ to a dynamic, mouldable system, emphasising that cognitive potential is not fixed at birth but continuously shaped by experience.
Kunsang Thungon· International Journal For Mu...· 0 citations
Conscious experience depends on the coordinated activity of neural processes that span multiple scales: from synapses to whole-brain dynamics. A recently introduced measure, dynamical independence (DI), identifies, characterises, and quantifies these multi-scale relationships using an information-theoretic dimensionality reduction approach. Here, we use DI to examine changes in the emergent dynamical organisation in the human brain under three pharmacologically-distinct anaesthetic interventions (propofol, xenon, ketamine). Applied to source-reconstructed electroencephalography (EEG), our analysis reveals that propofol and xenon, anaesthetics that abolish conscious report, exhibit more emergent but highly variable dynamic structure, indicating fragmented macroscopic dynamical organisation. Ketamine, which preserves dream-like phenomenology, shows a different pattern relative to wakefulness: reduced overall emergence yet a partial preservation of the macroscopic structure. Further exploratory analyses revealed spatially localised source-level contributions to emergent dynamical structure, highlighting regional variations. Together, our results highlight drug-induced reconfigurations of emergent dynamical structure relative to wakefulness, dissociate the amount of emergence from the organisation of emergent dynamics, and caution against equating emergence with level of consciousness. Consequently, we suggest that wakeful conscious processing depends not only on integration between neural components within a single scale, but also on integration across scales, broadening currently held assumptions of putative signatures of consciousness.
Borjan Milinkovic, A. Seth, Lionel Barnett et al.· Imaging Neuroscience· 0 citations
Making ISF available as a standalone online resource, it is believed it will facilitate the generation, simulation and analysis of models that reveal mechanistic origins of in vivo recorded activity beyond the barrel cortex for which it was originally designed.
B. Meulemeester, A. Bast, M. Royo et al.· PLoS Computational Biology· 0 citations
Astrocytes sense synaptic activity, neuromodulation, and metabolic signals, and respond by modulating neurotransmission, excitability, and plasticity in neural networks. Increasing evidence demonstrates that these processes contribute to information processing and encoding across brain areas, thereby influencing perception, memory, cognition, and goal-directed behaviours. Notably, impairments in these functions represent some of the earliest hallmarks of ageing and neurodegenerative disorders such as Alzheimer’s disease. Here we review molecular, cellular, and computational insights into astrocyte-neuron interactions, framing their importance at the system and behavioural level; then, we discuss the role of these interactions in spatial cognition, goal-directed behaviour, and their impairment in Alzheimer’s disease, and review the mouse models used to investigate spatial deficits and associated astrocyte activity. Finally, we highlight major open questions in the field, outline future research directions, and discuss emerging strategies to address astrocyte role in cognitive function in health and disease.
Marion Gaborit, Anahita Arabi, Letizia Mariotti· Frontiers in Cellular Neuros...· 0 citations
A computational model was developed in which GPe neurons are represented as coupled phase oscillators influenced by experimentally derived phase-response curves and extrinsic inputs, showing that while the model captures general trends, discrepancies exist in peak amplitude and decay rates, suggesting that key biological details of the GPe are not represented in the model.