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Decades of research have identified a role for dopamine neurotransmission in prefrontal cortical function and flexible cognition. Abnormal dopamine neurotransmission underlies many cases of cognitive dysfunction. New techniques using optogenetics have allowed for ever more precise functional segregation of areas within the prefrontal cortex, which underlie separate cognitive functions. Learning theory predictions have provided a very useful framework for interpreting the neural activity of dopamine neurons, yet even dopamine neurons present a range of responses, from salience to prediction error signaling. The functions of areas like the Lateral Habenula have been recently described, and its role, presumed to be substantial, is largely unknown. Many other neural systems interact with the dopamine system, like cortical GABAergic interneurons, making it critical to understand those systems and their interactions with dopamine in order to fully appreciate dopamine's role in flexible behavior. Advances in human clinical research, like exome sequencing, are driving experimental hypotheses which will lead to fruitful new research directions, but how do (or should?) these clinical findings inform basic research? Following new information from these techniques, we may begin to develop a fresh understanding of human disease states which will inform novel treatment possibilities. However, we need an operational framework with which to interpret these new findings. Therefore, the purpose of this Research Topic is to integrate what we know of dopamine, the prefrontal cortex and flexible behavior into a clear framework, which will illuminate clear, testable directions for future research.

behavioral flexibility --- Dopamine --- medial prefrontal cortex (mPFC) --- Attentional set-shifting --- basal forebrain --- anterior cingulate cortex (ACC) --- endocannabinoid system --- lateral habenula (LHb) --- Locus coeruleus (LC) --- motivational salience

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Anatomy of Neuropsychiatry: The New Anatomy of the Basal Forebrain and Its Implications for Neuropsychiatric Illness, Second Edition, builds upon reprised classic chapters by Lennart Heimer and Gary Van Hoesen describing the cortical and subcortical structure and functional involvements of several functional–anatomical macrosystems in the human forebrain, the existence of which obviates the vaunted heuristic value of the “limbic system” concept in the study of motivation and emotion. New narrative brings in important historical, philosophical, and histotechnical contexts, integration with novel technologies (e.g., optogenetics) and structures (e.g., rostromedial tegmental nucleus), a deeper dive into the interactions of forebrain and prospective cerebellar macrosystems with the reticular core of the brain, and current viewpoints on the essential role of macrosystems in motion, motivation, emotion, cognition, and neuropsychiatric well-being.

Neurobehavioral disorders --- Physiological aspects. --- Mental Disorders. --- Nervous System Diseases. --- Prosencephalon. --- Neuroanatomy. --- Neuropsychiatry. --- Nervous system --- Mental illness. --- Limbic Lobe --- Basal Forebrain --- Diseases. --- anatomy & histology --- anatomy & histology.

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This book covers the current trends in clinical deep brain stimulation (DBS) research. This collection of papers from experts in the field provides state of the art knowledge and future perspectives in clinical DBS research. A range of topics involved in DBS is presented, ranging from high resolution imaging, electrophysiology and personalized medicine, in a broad range of brain disorders.

Medicine --- deep brain stimulation --- Parkinson’s disease --- illness representations --- illness perceptions --- coping strategies --- microelectrode recordings --- subthalamic nucleus --- procedural sedation and analgesia --- clonidine --- dexmedetomidine --- remifentanil --- DBS --- tremor --- stimulation parameters --- DBS programming algorithm --- DBS side effects --- thalamic nucleus --- zona incerta --- closed loop --- sensing --- electrophysiology --- neurophysiology --- pain --- thermal grill --- imaging --- obsessive compulsive disorder --- cognitive behavioral therapy --- major depressive disorder --- treatment resistant depression --- neuropsychological subtypes --- personalized treatment approach --- treatment-resistant depression --- depression --- meta-analysis --- meta-regression --- subcallosal cingulate gyrus --- medial forebrain bundle --- inferior thalamic peduncle --- ventral capsule --- ventral striatum --- general anesthesia --- intraoperative computed tomography --- intraoperative magnetic resonance imaging --- local anesthesia --- microelectrode recording --- magnetic resonance imaging --- ultra-high field --- chronic pain --- lead externalization --- trial period --- stereoEEG --- subcallosal cingulate --- medial prefrontal cortex --- selection --- levodopa --- axial symptoms --- non motor symptoms --- genetics --- n/a --- Parkinson's disease

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Although sphingolipids are ubiquitous components of cellular membranes, their abundance in cells is generally lower than glycerolipids or cholesterol, representing less than 20% of total lipid mass. Following their discovery in the brain—which contains the largest amounts of sphingolipids in the body—and first description in 1884 by J.L.W. Thudichum, sphingolipids have been overlooked for almost a century, perhaps due to their complexity and enigmatic nature. When sphingolipidoses were discovered, a series of inherited diseases caused by enzyme mutations involved in sphingolipid degradation returned to the limelight. The essential breakthrough came decades later, in the 1990s, with the discovery that sphingolipids were not just structural elements of cellular membranes but intra- and extracellular signaling molecules. It turned out that their lipid backbones, including ceramide and sphingosine-1-phosphate, had selective physiological functions. Thus, sphingolipids emerged as essential players in several pathologies including cancer, diabetes, neurodegenerative disorders, and autoimmune diseases. The present volume reflects upon the unexpectedly eclectic functions of sphingolipids in health, disease, and therapy. This fascinating lipid class will continue to be the subject of up-and-coming future discoveries, especially with regard to new therapeutic strategies.

S1P receptor --- inflammation --- S1P transporter --- spinster homolog 2 --- barrier dysfunction --- anxiety --- depression --- sphingolipids --- sphingomyelinase --- ceramidase --- Smpd1 --- acid sphingomyelinase --- forebrain --- depressive-like behavior --- anxiety-like behavior --- ceramide --- ceramides --- ceramidases --- neurodegenerative diseases --- infectious diseases --- sphingosine 1-phoshate --- sphingosine 1-phosphate receptor --- S1P1–5 --- sphingosine 1-phosphate metabolism --- sphingosine 1-phosphate antagonistst/inhibitors --- sphingosine 1-phosphate signaling --- stroke --- multiple sclerosis --- neurodegeneration --- fingolimod --- Sphingosine-1-phosphate --- obesity --- type 2 diabetes --- insulin resistance --- pancreatic β cell fate --- hypothalamus --- sphingosine-1-phosphate --- ischemia/reperfusion --- cardioprotection --- vasoconstriction --- coronary flow --- myocardial function --- myocardial infarct --- albumin --- type 1 diabetes --- beta-cells --- islets --- insulin --- cytokines --- S1P --- animal models --- cystic fibrosis --- autophagy --- myriocin --- Aspergillus fumigatus --- CLN3 disease --- Cln3Δex7/8 mice --- flupirtine --- allyl carbamate derivative --- apoptosis --- cancer --- gangliosides --- immunotherapy --- metastasis --- phenotype switching --- sphingosine 1-phosphate --- Sphingosine 1-phosphate (S1P) --- S1P-lyase (SGPL1) --- tau --- calcium --- histone acetylation --- hippocampus --- cortex --- astrocytes --- neurons --- sphingosine kinase --- G-protein-coupled receptors --- Gαq/11 --- n/a --- sphingosine kinase 1 --- SK1 --- microRNA --- transcription factor --- hypoxia --- long non-coding RNA --- S1P1-5

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A revelatory tale of how the human brain develops, from conception to birth and beyondBy the time a baby is born, its brain is equipped with billions of intricately crafted neurons wired together through trillions of interconnections to form a compact and breathtakingly efficient supercomputer. Zero to Birth takes you on an extraordinary journey to the very edge of creation, from the moment of an egg’s fertilization through each step of a human brain’s development in the womb—and even a little beyond.As pioneering experimental neurobiologist W. A. Harris guides you through the process of how the brain is built, he takes up the biggest questions that scientists have asked about the developing brain, describing many of the thrilling discoveries that were foundational to our current understanding. He weaves in a remarkable evolutionary story that begins billions of years ago in the Proterozoic eon, when multicellular animals first emerged from single-cell organisms, and reveals how the growth of a fetal brain over nine months reflects the brain’s evolution through the ages. Our brains have much in common with those of other animals, and Harris offers an illuminating look at how comparative animal studies have been crucial to understanding what makes a human brain human.An unforgettable chronicle of one of nature’s greatest achievements, Zero to Birth describes how the brain’s incredible feat of orchestrated growth ensures that every brain is unique, and how breakthroughs at the frontiers of science are helping us to decode many traits that only reveal themselves later in life.

SCIENCE / Life Sciences / Neuroscience. --- Action potential. --- Agrin. --- Angiogenesis. --- Antibody. --- Apoptosis. --- Astrocyte. --- Axon guidance. --- Axon. --- Blastula. --- Brain asymmetry. --- Broca's area. --- Cancer cell. --- Cell type. --- Cerebral atrophy. --- Cerebral cortex. --- Charles Darwin. --- Chemical synapse. --- Critical period. --- Cyclopamine. --- Degenerative disease. --- Dendrite. --- Down syndrome. --- Ectoderm. --- Embryo. --- Embryology. --- Endocrinology. --- Eric Knudsen. --- Evolution. --- FOXP2. --- Filopodia. --- Forebrain. --- Ganglion cell. --- Gastrulation. --- Gene. --- Growth cone. --- Hans Spemann. --- Hebbian theory. --- Hindbrain. --- Hirschsprung's disease. --- Homeosis. --- Hox gene. --- Human brain. --- Immortalised cell line. --- John Gurdon. --- Lancelot Hogben. --- Lateralization of brain function. --- Marian Diamond. --- Midbrain. --- Model organism. --- Morphogen. --- Motor neuron. --- Muscle. --- Myocyte. --- Nematode. --- Nervous tissue. --- Neural crest. --- Neural development. --- Neural plate. --- Neural stem cell. --- Neural tube defect. --- Neural tube. --- Neuroblast. --- Neuroblastoma. --- Neuroepithelial cell. --- Neuroglia. --- Neuroimaging. --- Neuron doctrine. --- Neuron. --- Organoid. --- Petri dish. --- Progenitor cell. --- Proneural genes. --- Protein. --- Protocadherin. --- Purkinje cell. --- Reeler. --- Reelin. --- Renshaw cell. --- Reticular theory. --- Retinoic acid. --- Roel Nusse. --- Ross Granville Harrison. --- Sarcoma. --- Sonic hedgehog. --- Spina bifida. --- Spinal cord. --- Spindle apparatus. --- Stem cell. --- Sydney Brenner. --- Synapsis. --- Synaptic plasticity. --- Thomas Hunt Morgan. --- Thrombospondin. --- Torsten Wiesel. --- Transformation (genetics). --- Twin. --- Vertebrate. --- Visual word form area. --- White blood cell. --- Zygote. --- Brain --- Growth. --- Neuronal Plasticity --- SCIENCE / Life Sciences / Neuroscience --- SCIENCE / Life Sciences / Developmental Biology --- growth & development --- embryology --- physiology