About this Research Topic
Pathophysiological hyperactivity and hyperexcitability are observed in many different neurological disorders, including Epilepsy, Neurodegeneration, Neurodevelopmental disorders, Stroke, Retinal Degeneration, Tinnitus, and many more. In each case, the emergence of hyper-activity/excitability might be caused by different factors, and lead to different and varied consequences. However, in all cases, the uncontrolled firing of neurons in any part of the CNS is bound to disrupt existing circuits, deteriorate signal processing, and affect the excitation-to-inhibition (E/I) ratio. In some cases, compensatory mechanisms might be triggered to action, while in others they might fail to provide relief. Careful assessment of the commonalities and disparities in the mechanisms underlying neuronal hyperactivity in each pathology might provide the evidence necessary to uncover novel therapeutic targets and develop potential treatments.
The goal of this Research Topic is to share insights into the molecular and physiological sources of pathological hyperactivity, how it can be prevented or rescued, and whether antagonizing hyperactivity can improve disease outcome or mitigate specific phenotypes in-vitro or in-vivo. Special emphasis is put on the mechanism of disease and how it is linked to abnormal E/I ratio. By comparing different disease models using a wide spectrum of methodological approaches, we hope to build a body of knowledge that can lead to meaningful insights and conclusions, providing researchers in this field with a conceptual framework to advance the study of pathological hyperactivity and exchange ideas relevant to the topic.
In this Research Topic we welcome authors focusing on the following:
• Define hyperactivity and hyperexcitability in the context of a specific CNS disease, from neurodevelopmental disorders in embryonic life to age-related neurodegeneration. Layout specific hypotheses connecting the progression of the disease with the development of hyper-activity/excitability.
• Assess pre-synaptic and post-synaptic contributions to hyperactivity, identifying key players and focusing on specific brain regions, neural circuits, or neuronal subtypes, as well as clearly defined developmental and pathological stages.
• Discuss the ability of the disease model in use to approximate the pathology as seen in patients, and how well it recreates the hyperactivity and its molecular source. All relevant models will be considered, from in-vitro human neurons differentiated from stem cells to in-vivo behavioral studies in mammalians and other animals.
The goal of this Research Topic is to share insights into the molecular and physiological sources of pathological hyperactivity, how it can be prevented or rescued, and whether antagonizing hyperactivity can improve disease outcome or mitigate specific phenotypes in-vitro or in-vivo. Special emphasis is put on the mechanism of disease and how it is linked to abnormal E/I ratio. By comparing different disease models using a wide spectrum of methodological approaches, we hope to build a body of knowledge that can lead to meaningful insights and conclusions, providing researchers in this field with a conceptual framework to advance the study of pathological hyperactivity and exchange ideas relevant to the topic.
In this Research Topic we welcome authors focusing on the following:
• Define hyperactivity and hyperexcitability in the context of a specific CNS disease, from neurodevelopmental disorders in embryonic life to age-related neurodegeneration. Layout specific hypotheses connecting the progression of the disease with the development of hyper-activity/excitability.
• Assess pre-synaptic and post-synaptic contributions to hyperactivity, identifying key players and focusing on specific brain regions, neural circuits, or neuronal subtypes, as well as clearly defined developmental and pathological stages.
• Discuss the ability of the disease model in use to approximate the pathology as seen in patients, and how well it recreates the hyperactivity and its molecular source. All relevant models will be considered, from in-vitro human neurons differentiated from stem cells to in-vivo behavioral studies in mammalians and other animals.
Keywords: Pathological hyperactivity, neuronal computation, disease modeling, neuronal excitability, synaptic plasticity
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
