Homeostatic Control of Brain Function offers a broad view of brain health and diverse perspectives for potential treatments, targeting key areas such as mitochondria, the immune system, epigenetic changes, and regulatory molecules such as ions, neuropeptides, and neuromodulators. Loss of homeostasis becomes expressed as a diverse array of neurological disorders. Each disorder has multiple comorbidities - with some crossing over several conditions - and often disease-specific treatments remain elusive. When current pharmacological therapies result in ineffective and inadequate outcomes, therapies to restore and maintain homeostatic functions can help improve brain health, no matter the diagnosis. Employing homeostatic therapies may lead to future cures or treatments that address multiple comorbidities. In an age where brain diseases such as Alzheimer's or Parkinson's are ever present, the incorporation of homeostatic techniques could successfully promote better overall brain health. Key Features include · A focus on the homeostatic controls that significantly depend on the way one lives, eats, and drinks. · Highlights from emerging research in non-pharmaceutical therapies including botanical medications, meditation, diet, and exercise. · Incorporation of homeostatic therapies into existing basic and clinical research paradigms. · Extensive scientific basic and clinical research ranging from molecules to disorders. · Emerging practical information for improving homeostasis. · Examples of homeostatic therapies in preventing and delaying dysfunction. Both editors, Detlev Boison and Susan Masino, bring their unique expertise in homeostatic research to the overall scope of this work. This book is accessible to all with an interest in brain health; scientist, clinician, student, and lay reader alike.

Brain function is under metabolic control, which in turn determines the equilibrium of homeostatic systems that affect neuronal and glial networks on the molecular, cellular, and systems levels. The collection of articles ranges from molecules and mechanisms involved in regulating homeostasis and neuronal excitability to therapeutic mechanisms tailored to restore homeostatic function. It also features neurological diseases and novel treatment approaches that are based on metabolic and homeostatic interventions. Together, the collection of articles outlines novel strategies to restore brain function in neurology and highlights limitations of conventional pharmacological approaches. We suggest that restoration of molecular and biochemical networks could lead to a new era of therapeutic opportunities.

Cerebellum and Cerebrum in Homeostatic Control and Cognition presents a ground-breaking hybrid-brain psychology, proposing that the cerebellum and cerebrum operate in a complementary manner as equal cognitive partners in learning based control. The book synthesises contemporary neuroscience and psychology in terms of their common underlying control principle, homeostasis. Drawing on research and theory from neuroscience, psychology, AI and robotics, it provides a hybrid control systems interpretation of consciousness and self; unconscious mind; REM dream sleep; emotion; self-monitoring and self-control; memory, infantile amnesia; and, cognitive development. This is used to investigate different elements of cerebellum-cerebrum offline interaction; including attention and working memory, and explores cerebellar and cerebral contributions to various aspects of a number of disorders; including ADHD, ASD and schizophrenia. Presenting original ideas around neuropsychological architecture, the book will be of great interest to academics, researchers, and post-graduate students in the fields of neuropsychology, cognitive psychology, neuroscience and clinical psychology.

Several types of brain injuries are causes of acquired temporal lobe epilepsy (TLE). The seizure-free "latent period" that often follows the brain injury is of unknown mechanistic significance but is commonly considered as the "epileptogenic" period characterized by gradual pathogenic processes leading to the onset of clinically detectable epilepsy. Acute convulsive status epilepticus (SE) is often associated with an adverse developmental outcome characterized by learning disabilities related to the cumulative effects of seizures and development of TLE. The symptomatic manifestations of TLE appear only after a widespread irreversible damage of entorhinal cortex, and hippocampus, the brain area most affected by this disease. These pathological features of TLE reduce the possibility of successful therapeutic approaches, often rendering the disease refractory. The difficult clinical management of chronic TLE and the limited success rate of surgical approaches, increase the incapacitating nature of this specific epileptic disorder. Prevention of TLE with an appropriate intervention after a known inciting event (in the case of acquired epilepsy) might represent the most ambitious goal in the clinical treatment of this epileptic disorder, but has been largely unsuccessful to this point. Clinical trials aimed at prevention of chronic epilepsy have often produced negative, disappointing results. However, in most cases, these studies ultimately evaluated the downstream clinical manifestations, failing to monitor early, specific molecular epileptogenic events. Therefore, elucidation of the underlying mechanisms of epileptogenesis, and their time course(s) are essential. The primary purpose of this topic is to collect scientific contributions providing novel insights in the cellular and molecular mechanisms of epileptogenesis as potential targets for innovative therapeutic approaches aimed at preventing the chronic epileptic disorder.

The book presents a qualitative and quantitative approach to understanding, managing, and enforcing the integration of homeostasis in the human body. Homeostasis in the human body is very crucial, as it provides the basics of the normal functioning of the human body. Utilizing a sound theoretical and practical foundation and illustrating procedural techniques through scientific examples, this book bridges the gap between the need for understanding, utilizing, and going for detailed research in this aspect. Detailed procedures have been omitted because of the variety of equipment and commercial kits used in today’s clinical laboratories.

The field of autonomic neuroscience research concentrates on those neural pathways and processes that ultimately modulate parasympathetic and sympathetic output to alter peripheral organ function. In the following ebook, laboratories from across the field have contributed reviews and original research to summarize current views on the role of the brain in tuning peripheral organ performance to regulate body temperature, glucose homeostasis and blood pressure.

There is a growing appreciation that many psychiatric (and neurological) conditions can be understood as functional disconnection syndromes – as reflected in aberrant functional integration and synaptic connectivity. This Research Topic considers recent advances in understanding psychopathology in terms of aberrant effective connectivity – as measured noninvasively using functional magnetic resonance imaging (fMRI). Recently, there has been increasing interest in inferring directed connectivity (effective connectivity) from fMRI data. Effective connectivity refers to the influence that one neural system exerts over another and quantifies the directed coupling among brain regions – and how they change with pathophysiology. Compared to functional connectivity, effective connectivity allows one to understand how brain regions interact with each other in terms of context sensitive changes and directed coupling – and therefore may provide mechanistic insights into the neural basis of psychopathology. Established models of effective connectivity include psychophysiological interaction (PPI), structural equation modeling (SEM) and dynamic causal modelling (DCM). DCM is unique because it explicitly models the interaction among brain regions in terms of latent neuronal activity. Moreover, recent advances in DCM such as stochastic and spectral DCM, make it possible to characterize the interaction between different brain regions both at rest and during a cognitive task.

This illustrated handbook attempts to reconcile the quantitative, objective observations of Western Medicine with the qualitative, subjective observations of Eastern Yoga.

Activity within neural circuits shapes the synaptic properties of component neurons in a manner that maintains stable excitatory drive, a process referred to as homeostatic plasticity. These potent and adaptive mechanisms have been demonstrated to modulate activity at the level of an individual neuron, synapse, circuit, or entire network, and dysregulation at some or all of these levels may contribute to neuropsychiatric disorders, intellectual disability, and epilepsy. Greater mechanistic understanding of homeostatic plasticity will provide key insights into the etiology of these disorders, which may result from network instability and synaptic dysfunction. Over the past 15 years, the molecular mechanisms of this form of plasticity have been intensely studied in various model organisms, including invertebrates and vertebrates. Though once thought to have a predominantly postsynaptic basis, emerging evidence suggests that homeostatic mechanisms act on both sides of the synapse through mechanisms such as retrograde signaling, to orchestrate compensatory adaptations that maintain stable network function. These trans-synaptic signaling systems ultimately alter neurotransmitter release probability by a variety of mechanisms including changes in vesicle pool size and calcium influx. These adaptations are not expected to occur homogenously at all terminals of a pre-synaptic neuron, as they might synapse with neurons in non-overlapping circuits. However, the factors that govern the homeostatic control of synapse-specific plasticity are only beginning to be understood. In addition to our limited molecular understanding of pre-synaptic homeostatic plasticity, very little is known about its prevalence in vivo or its physiological and disease relevance. In this research topic, we aim to fill the aforementioned void by covering a broad range of topics that include: - Identification of signaling pathways and mechanisms that operate globally or locally to induce specific pre-synaptic adaptations - The nature of pre-synaptic ion channels relevant to this form of plasticity and their synapse-specific modulation and trafficking - Development and utilization of new tools or methods to study homeostatic plasticity in axons and pre-synaptic terminals - Novel mechanisms of homeostatic adaptations in pre-synaptic neurons - Postsynaptic sensors of activity and retrograde synaptic signaling systems - A comprehensive analysis of the kinds of pre-synaptic adaptations in diverse neural circuits and cell types - Identification of physiological or developmental conditions that promote pre-synaptic homeostatic adaptations - How activity-dependent (Hebbian) and homeostatic synaptic changes are integrated to both permit sufficient flexibility and maintain stable activity - Relevance of pre-synaptic homeostatic plasticity to the etiology of neuropsychiatric disorders - Computational modeling of pre-synaptic homeostatic plasticity and network stability.