Since the pioneering discovery of cyclic AMP four decades ago, a multitude of signaling pathways have been uncovered in which an extracellular signal (first messenger) impacts the cell surface, thereby triggering a cascade that ultimately acts on the cell nucleus. In each cascade the first messenger gives rise to the appearance of a second messenger such as cyclic AMP, cyclic GMP, or diacylglycerol, which in turn triggers a third messenger, a fourth messenger, and so forth. Many advances in elucidating such pathways have been made, including efforts to link messenger molecules to brain processes operative in health or disease. However, the latter type of information, relating signaling pathways to brain function, is scattered across a variety of publication media, which makes it difficult to integrate the multiple roles of different signaling cascades into our understanding of brain function in health and disease. The primary aim of Cerebral Signal Transduction: From First to Fourth Messengers, therefore, is to offer a comprehensive picture of the recent advances made in the signaling field as it relates to neuronal and cere bral function. The current state of progress provides an exciting opportunity for such a comprehensive focus because molecular tools have become available to selectively remove, reduce, or enhance spe cific components in the signaling pathways, e. g. , by interfering with the genes encoding key proteins. In addition, the increased awareness of crosstalk between different signaling cascades has revealed many possibilities for changes in gene expression underlying long-term changes in brain function.

An illuminating summary of our current understanding of the interactive role of dopamine and glutamate in psychiatric diseases and the therapeutic strategies and possibilities for future treatment. Among the new ideas presented are hypotheses on the role of dopamine and glutamate in aggression, the glutamate system in anxiety disorders, glutamate and neurodegeneration, and on the origin and progression of Parkinson's disease. Additional chapters offer novel insights into a variety of psychiatric diseases, including ADHD, stress, aggression, addiction, schizophrenia, depression, social phobias, dementias, bulimia, and neurodegenerative diseases like Parkinson's and Alzheimer's diseases. Each chapter summarizes the prevalence and symptoms of the disease and explains the involvement of dopamine and/or glutamate systems using the newer molecular approaches such as transgenic knockout or knockin mice and recent brain imaging techniques.

Neurotransmission is a multicomponent process. Transmitters, released by neuronal activity, act on pre- and postsynaptic receptors, and many books detail advances in the receptor field. In addition, after their release from nerve endings, transmitters are removed from the neuronal vicinity by uptake into neuronal or glial cells by specific tra- porter proteins that have been studied intensely over the last 30 years; this information is scattered throughout numerous publishing vehicles. Therefore, the primary aim of this second edition of N- rotransmitter Transporters: Structure, Function, and Regulation is to offer a comprehensive picture of the characterization of neurotransmitter transporters and their biological roles. The transporter field has moved forward in stages. In the first phase, progress came from the use of substrate or blocker ligands selectively targeting transporters, the application of model systems allowing the study of transmitter tra- port shielded from storage, and the development of mathematical models for describing transport phenomena. In the second phase, roughly covering the last decade, advances in DNA techniques allowed the cloning of numerous genes coding for different transporter proteins. In the current, third stage, a wealth of information is being accumulated in studies relating transporter structure with function, experiments addressing regulation by posttranslational transfor- tion, investigations into transport modulation by trafficking processes and genomic influences, characterization of channel properties of tra- porters by electrophysiological approaches, and the creation of transgenic animals under- or overexpressing a given transporter protein.

An illuminating summary of our current understanding of the interactive role of dopamine and glutamate in psychiatric diseases and the therapeutic strategies and possibilities for future treatment. Among the new ideas presented are hypotheses on the role of dopamine and glutamate in aggression, the glutamate system in anxiety disorders, glutamate and neurodegeneration, and on the origin and progression of Parkinson's disease. Additional chapters offer novel insights into a variety of psychiatric diseases, including ADHD, stress, aggression, addiction, schizophrenia, depression, social phobias, dementias, bulimia, and neurodegenerative diseases like Parkinson's and Alzheimer's diseases. Each chapter summarizes the prevalence and symptoms of the disease and explains the involvement of dopamine and/or glutamate systems using the newer molecular approaches such as transgenic knockout or knockin mice and recent brain imaging techniques.

Neurotransmission is a multicomponent process. Transmitters, released by neuronal activity, act on pre- and postsynaptic receptors, and many books detail advances in the receptor field. In addition, after their release from nerve endings, transmitters are removed from the neuronal vicinity by uptake into neuronal or glial cells by specific tra- porter proteins that have been studied intensely over the last 30 years; this information is scattered throughout numerous publishing vehicles. Therefore, the primary aim of this second edition of N- rotransmitter Transporters: Structure, Function, and Regulation is to offer a comprehensive picture of the characterization of neurotransmitter transporters and their biological roles. The transporter field has moved forward in stages. In the first phase, progress came from the use of substrate or blocker ligands selectively targeting transporters, the application of model systems allowing the study of transmitter tra- port shielded from storage, and the development of mathematical models for describing transport phenomena. In the second phase, roughly covering the last decade, advances in DNA techniques allowed the cloning of numerous genes coding for different transporter proteins. In the current, third stage, a wealth of information is being accumulated in studies relating transporter structure with function, experiments addressing regulation by posttranslational transfor- tion, investigations into transport modulation by trafficking processes and genomic influences, characterization of channel properties of tra- porters by electrophysiological approaches, and the creation of transgenic animals under- or overexpressing a given transporter protein.

Since the pioneering discovery of cyclic AMP four decades ago, a multitude of signaling pathways have been uncovered in which an extracellular signal (first messenger) impacts the cell surface, thereby triggering a cascade that ultimately acts on the cell nucleus. In each cascade the first messenger gives rise to the appearance of a second messenger such as cyclic AMP, cyclic GMP, or diacylglycerol, which in turn triggers a third messenger, a fourth messenger, and so forth. Many advances in elucidating such pathways have been made, including efforts to link messenger molecules to brain processes operative in health or disease. However, the latter type of information, relating signaling pathways to brain function, is scattered across a variety of publication media, which makes it difficult to integrate the multiple roles of different signaling cascades into our understanding of brain function in health and disease. The primary aim of Cerebral Signal Transduction: From First to Fourth Messengers, therefore, is to offer a comprehensive picture of the recent advances made in the signaling field as it relates to neuronal and cere bral function. The current state of progress provides an exciting opportunity for such a comprehensive focus because molecular tools have become available to selectively remove, reduce, or enhance spe cific components in the signaling pathways, e. g., by interfering with the genes encoding key proteins. In addition, the increased awareness of crosstalk between different signaling cascades has revealed many possibilities for changes in gene expression underlying long-term changes in brain function."