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Glutamic acid --- Glutamate --- Excitatory amino acids --- Umami (Taste) --- Metabolism. --- Physiological effect.

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Neuropsychiatric disorders, covering both psychotic and depressive disorders, but also autism and attention-deficit hyperactivity disorder (ADHD), are characterized by abnormal behavior and brain structure. Accumulating evidence suggests that altered neurochemistry plays a role in these disorders and may have a causal relationship with the observed behavioral and structural abnormalities. To improve the understanding of neurochemical anomalies and (patho)physiological changes in psychiatric conditions, in vivo assessment of the affected tissue, the brain, is wanted and needed. Magnetic resonance spectroscopy (MRS) is a non-invasive technique which allows in vivo assessment of the molecular composition of brain tissues and identification of metabolites involved in physiological and pathological processes, which is otherwise virtually impossible. Only in the last decade with the development of high field MR methodologies, MRS has become sensitive enough for broader use in clinical studies. The implications are many, but proper guidance and elucidation of the pros and cons for the specific methods is needed to optimally exploit the potential. This Research Topic updates the reader on the possibilities and pitfalls of MRS today and highlights methodologies and applications for the future.

Neurochemistry --- Neuroimaging --- Schizophrenia --- GABA --- 7 Tesla MRI --- Glutamate --- Functional MRS --- Psychiatry --- MR spectroscopy

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Proteolysis by the ubiquitin-proteasome pathway (UPP) in the nervous system has been extensively studied both in the context of normal physiological function as well as abnormal pathological conditions. Although ubiquitin was used as a marker of brain pathology, the normal functions of the UPP were not studied much in the nervous system until the 1990s. The early investigations focused on synaptic plasticity which was followed by studies on the roles of protein degradation in the development of the nervous system. Research on the role of abnormal roles of the UPP follows a parallel trajectory. Since the 2000s, the field has grown to encompass many subareas of research and several model systems. Despite the progress made, many unanswered questions still remain. For example, there are many unknowns about the precise spatial and temporal control of protein degradation in the normal nervous system. With respect to the roles of proteolysis in brain pathology a major challenge is to elucidate the connection between impaired protein degradation and disease progression. In addition, in-depth studies of the roles of ubiquitin-proteasome-mediated proteolysis in neurodegenerative diseases are promising in identifying therapeutic targets. This ebook contains original research papers and insightful reviews that cover several aspects of proteolysis by the UPP and its physiological as well as pathological functions in the nervous system.

proteasome --- memory --- neuroinflammation --- neurodegenerative --- synaptic plasticity --- aging --- deubiquitinating --- Huntington's disease --- Alzheimer's disease --- glutamate receptors

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

metabotropic glutamate receptors --- neurological disorders --- psychiatric disorders --- Neuroprotection --- Neuroinflammation --- excitotoxicity --- Neurogenesis --- Positive allosteric modulators --- negative allosteric modulators

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One research field that early recognized the importance of intercellular interactions was endocrinology, initially in processes involved in lactation, pubertal maturation and regulation of the female ovarian cycle and later in appetite regulation. These interactions included, but were not restricted to neuronal-astrocytic interactions. The importance of glutamatergic and GABAergic signaling during all of these events is now realized. At the same time huge advances have been made in i) determination of metabolic rates in the human and rodent brain in vivo, including oxidative metabolism rates in astrocytes which per volume are at par with those in neurons; ii) understanding the unique ability of astrocytes, but not neurons to synthetize tricarboxylic acid intermediates necessary for net synthesis of glutamate and thereby also GABA; iii) determination of the rates at which such synthesis occurs, and iv) the two-fold higher rates at which glutamate and GABA are cycled between astrocytes and neurons in the brain in vivo. This quantitative difference reflects that most transmitter uptake, especially that of glutamate, occurs in astrocytes and that on average two thirds of astrocytically accumulated neuronal transmitters are recycled to neurons, whereas the last one third is oxidatively degraded, mainly or exclusively in astrocytes. The progress in these areas puts emphasis on i) firmly establishing whether or not aralar, a necessary component of the aspartate/glutamate exchanger in the malate-aspartate cycle is expressed in astrocytes, and ii) the detailed processes occurring in astrocytes and in neurons during the formation and subsequent oxidative degradation of transmitter glutamate and GABA. Initial observations by different groups showed no astrocytic aralar expression in mature brain. However, a recent paper by Pardo et al. (J. Cereb Blood Flow & Met.) used improved cytochemical techniques and showed some protein expression in astrocytes in mature brain; Hertz (same journal) calculated that the amount would be sufficient for normal oxidative degradation. However, there are indications that the astrocytic-neuronal-astrocytic interactions in formation, transfer and re-oxidation of transmitter glutamate and GABA may repeatedely require additional MAS function. Equal expression of aralar mRNA has been shown by the Nedergaard group in neurons and astrocytes obtained by fluorescence-activated cell sorting of brain cells from mice co-expressing astrocytic and neuronal markers with different fluorescent signals. This has recently been confirmed and also shown to be the case for aralar protein (J. Neurochem, under revision).

Endocrinology. --- Brain glutamine --- brain metabolism --- Appetite Regulation --- Astrocyte-oligdendrocyte interaction --- Brain ammonia --- GABA --- Astrocytic gene expression --- pancreatic islets --- Brain aspartate --- Brain glutamate