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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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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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The present studies evaluated the effect of chronic intraventricular microinfusion of norepinephrine (NE) to examine if higher levels of intracerebral NE could protect against the development of delayed neuronal death (DND) in the hippocampus of a transient forebrain ischaemia model. Small cannulas connected to osmotic minipumps were stereotactically placed in the lateral ventricle, and NE (40 mu M) was pumped at the rate of 0.5 mu l/hour for periods of up to 14 days. Brain tissue was then analysed for the total NE content at 2.5 mm intervals from the cannula tip, using high pressure liquid chromatography, The result of these preliminary studies showed a 5 to 40-fold increase in the NE levels in the specimens on the infusion side and a 2 to 3-fold increase on the non-infusion side. The number of surviving pyramidal neurones in the hippocampal CA1 region were then compared between the ipsilateral and contralateral hemispheres of the brains obtained from experimental and control animals. Significant suppression of neuronal death was demonstrated in the presence of increased levels of exogenous NE on the infusion side. These studies suggest that intraventricular administration of NE is feasible and that the resulting higher levels of NE may attenuate the phenomenon of DND in the hippocampus, possibly by a direct protective action upon the neurones

Animal. --- Animals. --- Brain. --- Ca1. --- Cannula. --- Control. --- Damage. --- Death. --- Delayed neuronal death. --- Density. --- Development. --- Forebrain ischemia. --- Gerbil hippocampus. --- Hemisphere. --- Hippocampal. --- Hippocampus. --- Increase. --- Injury. --- Ischaemia. --- Ischemic brain. --- Level. --- Locus coeruleus. --- Model. --- Neuronal death. --- Neuronal. --- Norepinephrine. --- Periods. --- Production. --- Rat. --- Suppression. --- Time. --- Transient ischemia.

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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