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In the first 20 years that followed the purinergic signalling hypothesis in 1972, most scientists were sceptical about its validity, largely because ATP was so well established as an intracellular molecule involved in cell biochemistry and it seemed unlikely that such a ubiquitous molecule would act as an extracellular signalling molecule. However, after the receptors for ATP and adenosine were cloned and characterized in the early 1990s and ATP was established as a synaptic transmitter in the brain and sympathetic ganglia, the tide turned. More recently it has become clear that ATP is involved in long-term (trophic) signalling in cell proliferation, differentiation and death, in development and regeneration, as well as in short-term signalling in neurotransmission and secretion. Also, important papers have been published showing the molecular structure of P2X receptors in primitive animals like Amoeba and Schistosoma, as well as green algae. This has led to the recognition of the widespread nature of the purinergic signalling system in most cell types and to a rapid expansion of the field, including studies of the pathophysiology as well as physiology and exploration of the therapeutic potential of purinergic agents. In two books, Geoffrey Burnstock and Alexej Verkhratsky have aimed at drawing together the massive and diverse body of literature on purinergic signalling. The topic of this first book is purinergic signalling in the peripheral and central nervous systems and in the individual senses. In a second book the authors focus on purinergic signalling in non-excitable cells, including those of the airways, kidney, pancreas, endocrine glands and blood vessels. Diseases related to these systems are also considered.
In the first 20 years that followed the purinergic signalling hypothesis in 1972, most scientists were sceptical about its validity, largely because ATP was so well established as an intracellular molecule involved in cell biochemistry and it seemed unlikely that such a ubiquitous molecule would act as an extracellular signalling molecule. However, after the receptors for ATP and adenosine were cloned and characterized in the early 1990s and ATP was established as a synaptic transmitter in the brain and sympathetic ganglia, the tide turned. More recently it has become clear that ATP is involved in long-term (trophic) signalling in cell proliferation, differentiation and death, in development and regeneration, as well as in short-term signalling in neurotransmission and secretion. Also, important papers have been published showing the molecular structure of P2X receptors in primitive animals like Amoeba and Schistosoma, as well as green algae. This has led to the recognition of the widespread nature of the purinergic signalling system in most cell types and to a rapid expansion of the field, including studies of the pathophysiology as well as physiology and exploration of the therapeutic potential of purinergic agents. In two books, Geoffrey Burnstock and Alexej Verkhratsky have aimed at drawing together the massive and diverse body of literature on purinergic signalling. The topic of this first book is purinergic signalling in the peripheral and central nervous systems and in the individual senses. In a second book the authors focus on purinergic signalling in non-excitable cells, including those of the airways, kidney, pancreas, endocrine glands and blood vessels. Diseases related to these systems are also considered.
This Research Topic aims to honour the 80th birthday of Professor Peter Illes, who is a member of the European Academy of Sciences, the founder/first president of the German Purine Club, and Honorary President of the Chinese Purine Club. He established a worldwide co-operation network on purinergic signalling and is an internationally recognized leader in the field. We aim to collect research articles and reviews from friends, colleagues and co-operation partners of Dr. Illes to showcase, build on and develop research being achieved related to the physiological/pathophysiological roles of purines in the central nervous system (CNS). Adenosine Triphosphate (ATP) is an intracellular energy-storing molecule, but may also reach the extracellular space, where it participates in cell-to-cell signalling. For this purpose, ATP utilises a range of purinergic receptors activated either by ATP itself (P2X receptors; seven subtypes) or by ATP/ADP and UTP/UDP (P2Y receptors; 8 subtypes) and finally via its enzymatic degradation product, adenosine (P1/A receptors; 4 subtypes). Purine nucleotides and nucleosides together with the whole plethora of receptors and degrading enzymes constitute the purinome. This fascinating and extensive network exists both in the animal kingdom and in humans and is essential in regulating important physiological functions. Disturbances in the network can lead to a variety of illnesses clinically associated with both neurological or psychiatric traits. In recent years, hope has arisen that pharmacological chemistry together with various newly developed methods, will enable researchers to discover and design efficient drugs for treating these neurodegenerative and affective diseases.
ATP, the intracellular energy source, is also an extremely important cell–cell signalling molecule for a wide variety of cells across evolutionarily diverse organisms. The extracellular biochemistry of ATP and its derivatives is complex, and the multiple membrane receptors that it activates are linked to many intracellular signalling systems. Purinergic signalling affects a diverse range of cellular phenomena, including ion channel function, cytoskeletal dynamics, gene expression, secretion, cell proliferation, differentiation and cell death. Recently, this class of signalling molecules and receptors has been found to mediate communication between neurons and non-neuronal cells (glia) in the central and peripheral nervous systems. Glia are critical for normal brain function, development and response to injury. Neural impulse activity is detected by glia and purinergic signalling is emerging as a major means of integrating functional activity between neurons, glia and vascular cells in the nervous system. These interactions mediate effects of neural activity on the development of the nervous system and in association with injury, neurodegeneration, myelination and cancer. Bringing together contributions from experts in diverse fields, including glial biologists, neurobiologists and specialists in purinergic receptor structure and pharmacology, this book considers how extracellular ATP acts to integrate communication between different types of glia, and between neurons and glia. Beginning with an overview of glia and purinergic signalling, it contains detailed coverage of purine release, receptors and reagents, purinergic signalling in the neural control of glial development, glial involvement in information processing, and discussion of the interactions between neurons and microglia.
Gliomas, developing in the brain from the transformed glial cells, are a very special kind of tumor, extremely refractory to conventional treatments. Therefore, for the development of new antitumor strategies, a better understanding of molecular mechanisms responsible for their biology, growth and invasion is still needed. This book is a reference on cellular signaling processes regulating gliomas physiology and invasiveness. The work is focused on the mechanism of nucleotide receptor activation by exogenous nucleotides and formation of complex signaling cascades induced by growth factors, cytokines and cannabinoids. The second edition of the book enriched in new chapters provides a framework explaining how signal transduction elements may modulate numerous genetic and epigenetic alterations, describes the role of local microenvironment in cellular growth, progression and invasion and, in the light of extensive new results, presents perspectives concerning potential targets for gliomas therapy.
Since their discovery approximately 25 years ago, adenosine receptors have now emerged as important novel molecular targets in disease and drug discovery. These proteins play important roles in the entire spectrum of disease from inflammation to immune suppression. Because of their expression on a number of different cell types and in a number of different organ systems they play important roles in specific diseases, including asthma, rheumatoid arthritis, Parkinson’s disease, multiple sclerosis, Alzheimer’s disease, heart disease, stroke, cancer, sepsis, and obesity. As a result of intense investigations into understanding the molecular structures and pharmacology of these proteins, new molecules have been synthesized that have high specificity for these proteins and are now entering clinical trials. These molecules will define the next new classes of drugs for a number of diseases with unmet medical needs.
Adenosine 5'-triphosphate (ATP) is one of the most abundant molecule in living cells serving as universal energy "currency." After slow acceptance of the concept of the release and extracellular action of ATP, purinergic signaling is recognized as a widespread mechanism for cell-to-cell communication in living organisms. Additionally, the contribution of pyrimidine nucleotides (such as UTP and UDP) and sugar-nucleotides (i.e., UDP-glucose and UDP-galactose) have been more recently discovered. Purinergic signaling plays major physiological roles in mammalian central nervous system (CNS) such as neurotransmission, neuromodulation, communication in glial network and between neurons and glia. Extracellular ATP and its metabolic breakdown is a source of other nucleotides and adenosine providing the versatile basis for complex purinergic signaling through the activation of several families of purinergic receptors. G-protein coupled P1 receptors for adenosine, ionotropic P2X receptors for ATP and G-protein coupled P2Y receptors for ATP and other nucleotides are abundant and widely distributed in central neurons at pre-and post-synapse and in glial cells. Alterations of purinergic signals are associated with major CNS disorders including chronic pain, brain trauma ischemia, epilepsy, neurodegenerative diseases such as Alzheimer disease or Amyotrophic lateral sclerosis associated with neuro-inflammation as well as neuropsychiatric diseases, including depression, anxiety and schizophrenia.
This volume explores the quickly evolving field of Purinergic signaling, and examines how receptors for ATP and other nucleotides, and receptors for adenosine, act in neuronal transmission, control of synaptic activity, proliferation, differentiation and cell death regulation in the CNS. This book focuses on the participation of purinergic receptors and ectonucleotidases, degrading ATP into adenosine, in embryonic and adult neurogenesis in vitro and in vivo as well as in synaptic transmission and pathophysiology. Further, the chapters discuss varying brain diseases, including Parkinson’s, and Alzheimer’s disease, autism, mood disorders and epilepsy, as well as brain tumors, in the context of purinergic signaling and its clinical aspects. The development of purinergic receptor agonists is also an important issue of this book. This book provides a critical review of the current state of science and will be useful for both scientists and students who are or would like to get involved in this area. Furthermore, this book addresses neuroscientists, physician and professionals from the industry, who would like to update themselves in this exciting and rapidly growing field of neuroscience.
In this book we attempt a synthesis of knowledge from two investigative extremes. On the one hand, neurophysiology and neuropharmacology are progressing via the single neuron to a subcellular level; on the other, clinicians are studying the function ofthe human urinary system in vivo as a whole. A special effort must be made over the next decade to bridge this gap. We hope that the information summarized here will catalyse the process. In 1968, de Groat and Ryall published a group of papers in the Journal of Physiology in which modern quantitative electrophysiological techniques were applied to the study ofthe reflexes that regulate bladder Junction. These papers represent alandmark in the history of bladder neurophysiology, forming a dividing li ne between old and new. The earlier techniques of lesioning and stimulation of nervous structures yielded mainly qualitative information which was open to criticism because of lack of precise control over what was actually being destroyed or stimulated. Much of this earlier work was reviewed in an authoritative volume by Bors and Comarr in 1971, entitled Neurolqgical Urology. The 16 years have seen great advances in our understanding ofthe control oflower subsequent urinary tract function.