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1
Hardcastle, Valerie Gray. "The nontrivial doctrine of cognitive neuroscience." Behavioral and Brain Sciences 22, no. 5 (1999): 839. http://dx.doi.org/10.1017/s0140525x99322196.
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Gold & Stoljar's “trivial” neuron doctrine is neither a truism in cognitive science nor trivial; it has serious consequences for the future direction of the mind/brain sciences. Not everyone would agree that these consequences are desirable. The authors' “radical” doctrine is not so radical; their division between cognitive neuroscience and neurobiology is largely artificial. Indeed, there is no sharp distinction between cognitive neuroscience and other areas of the brain sciences.
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Reese, Benjamin. "Visual Neuroscience is turning twenty." Visual Neuroscience 25, no. 1 (2008): 1. http://dx.doi.org/10.1017/s0952523808080127.
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Your journal enters its third decade with the publication of this issue. The first volume, published in 1988, appeared in quarterly issues, but moved to bi-monthly production in 1989, and then monthly release from 1990 through 1992. Two volumes appeared each year during 1989–1992, accounting for the fact that this twenty-first year coincides with volume 25. In 1993, it returned to bi-monthly publication, remaining so for the past 15 years. During this period, other vision-related journals have made their debut, but Visual Neuroscience remains a premier venue for publishing fundamental research in the neurobiology of vision.
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Shibkova, Dariya Zakharovna, and Pavel Azifovich Baiguzhin. "NEUROSCIENCE: INTERDISCIPLINARY INTEGRATION OR EXPANSION?" Психология. Психофизиология 13, no. 3 (2020): 111–21. http://dx.doi.org/10.14529/jpps200312.
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Aim. The paper aims to study the differentiation and integration of scientific disciplines in the natural sciences and humanities research areas of neuroscience based on a review of Russian scientific works and to propose a structural and functional model of neuroscience as an interdisciplinary system of knowledge about brain features that ensure human activity in various professional spheres. Methods. A theoretical analysis of scientific publications on the topic over the last ten years has been used along with such methods as comparison, generalization, and modelling. Results. The paper presents various points of view on the subject field of separate disciplines within neuroscience, as well as on the relations between them. The interdisciplinarity of neuroscience is considered by a number of authors (philosophers) as a form of disciplinary colonization, epistemic expansion or intervention. Another group of authors considers neuroscience as a systemic level of science that unites multidisciplinary research activities related to the study of the brain. The third position is represented by authors who consider neuroscience as an extension of the problem field of neurobiology or as its synonym. A number of authors pay special attention to the popularity of neuroscience among politicians, military structures, pharmacological companies and other professionals with their disciplinary totality: neurophilosophy, neuropsychology, neuroinformatics, neurogenetics, neurobiology, neurosociology, neuropedagogy, etc. The paper demonstrates that there is no unified point of view on psychophysiology as a part of neuroscience, which also has interdisciplinary connections with many sciences that study individual psychological characteristics and behavior. Conclusion. Based on the analysis of the discussion, the authors emphasize the need to logically build the structural and functional relationships of individual disciplines within a unified neuroscience and determine its subject field on the basis of a systemic evolutionary approach.
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Keverne, Eric B. "GABA-ergic neurons and the neurobiology of schizophrenia and other psychoses." Brain Research Bulletin 48, no. 5 (1999): 467–73. http://dx.doi.org/10.1016/s0361-9230(99)00025-8.
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Huffard, Christine L. "Cephalopod neurobiology: an introduction for biologists working in other model systems." Invertebrate Neuroscience 13, no. 1 (2013): 11–18. http://dx.doi.org/10.1007/s10158-013-0147-z.
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Nishino, Seiji, and Emmanuel Mignot. "Neurobiology of Narcolepsy." Neuroscientist 4, no. 2 (1998): 133–43. http://dx.doi.org/10.1177/107385849800400209.
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Narcolepsy is characterized by excessive daytime sleepiness and abnormal rapid eye movement sleep. It affects about 0.05% of the Caucasian population. Human narcolepsy involves the interaction of environmental factors with a specific immunogenetic background. It is tightly associated with a major histocompatibility complex allele, human leukocyte antigen (HLA) DQB1*0602. Genetic factors other than HLA are also involved. In contrast, narcolepsy in Dobermans is transmitted as a single autosomal recessive trait. This canine narcolepsy gene is unlinked to the major histocompatibility complex class II but co-segregates with a DNA segment with high homology to the human immunoglobulin μ-switch sequence, further suggesting immunopathology in narcolepsy. However, attempts to demonstrate that narcolepsy is an autoimmune disease have been unsuccessful. Narcolepsy is treated with antidepressants for rapid eye movement sleep-related symptoms and with amphetamine-like stimulants for sleepiness. Pharmacological studies using narcoleptic canines indicate that monoaminergic and cholinergic systems are involved in the pathophysiology of narcolepsy. Dopaminergic uptake mechanisms and D2(3) autoreceptors are involved in the control of alertness, whereas adrenergic uptake mechanisms, α-1 and α-2/dopaminergic D2(3) receptors, are involved in the control of cataplexy, suggesting that amphetamine-like stimulants act via the dopaminergic system and that antidepressants exhibit their anticataplectic effects via the adrenergic system. Local drug perfusion studies indicate that D2(3) agonists in the ventral tegmental area induce cataplexy and sleepiness in narcoleptic dogs but not in control dogs. Furthermore, perfusion of M2 agonists in the pontine reticular formation and the basal forebrain induces cataplexy in narcoleptic dogs. Extracellular single-unit and acetylcholine measurement studies suggest that basal forebrain cholinoceptive sites mediate the emotional trigger for cataplexy. Although narcolepsy does not seem to be a classical autoimmune disease, concomitant increases in microglial HLA class II expression with the development of the disease occur in canine narcolepsy. A neuroimmune-related process at an early age is thus likely to contribute to the neurochemical imbalance seen in narcolepsy. NEUROSCIENTIST 4:133–143, 1998
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Schilbach, Leonhard. "Towards a second-person neuropsychiatry." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1686 (2016): 20150081. http://dx.doi.org/10.1098/rstb.2015.0081.
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Psychiatric disorders can affect our ability to successfully and enjoyably interact with others. Conversely, having difficulties in social relations is known to increase the risk of developing a psychiatric disorder. In this article, the assumption that psychiatric disorders can be construed as disorders of social interaction is reviewed from a clinical point of view. Furthermore, it is argued that a psychiatrically motivated focus on the dynamics of social interaction may help to provide new perspectives for the field of social neuroscience. Such progress may be crucial to realize social neuroscience's translational potential and to advance the transdiagnostic investigation of the neurobiology of psychiatric disorders.
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Miller, Raissa M., and Casey A. Barrio Minton. "Experiences Learning Interpersonal Neurobiology: An Interpretative Phenomenological Analysis." Journal of Mental Health Counseling 38, no. 1 (2016): 47–61. http://dx.doi.org/10.17744/mehc.38.1.04.
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Neuroscience is increasingly part of the national dialogue regarding mental health and yet little is known about the experiences of mental health professionals learning and integrating neuroscience into their work. In this study, the authors explored mental health professionals' experiences learning Interpersonal Neurobiology (IPNB). Four super-ordinate themes emerged from an interpretative phenomenological analysis: (1) learning process as dynamic and engaging, (2) deepening knowledge and understanding of self and others, (3) personal and professional growth, and (4) impact on therapeutic practice. Three higher-order constructs appeared embedded within and across themes: learning as ongoing, person of the participant, and person of the instructor. These findings suggest learning IPNB through experiential-based means had a profound impact on participants' personal and professional development, specifically in areas related to characteristics of effective counselors. Implications for future research and mental health practice are discussed.
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Weissensteiner, Elisabeth, and Dorothea Brückner. "Mirror Brain: Picture and Experience." Leonardo 47, no. 3 (2014): 216–24. http://dx.doi.org/10.1162/leon_a_00678.
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The installation Mirror Brain was developed by artist Elisabeth Weissensteiner and neurobiologist Dorothea Brückner at the University of Bremen, Germany, where it was launched. The installation, a contemporary work of hybrid art, establishes a philosophical play with viewers-turned-actors rather than an interpretation of neuroscience. Thus it provides a metaphor—a mirro—for the role of neurobiology in science and in art. Based on the project, this paper elaborates on how artistic and scientific depiction differ from each other.
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Kanske, Philipp, and Ryan J. Murray. "Understanding others: The neurobiology of social cognition." Cortex 121 (December 2019): A1—A2. http://dx.doi.org/10.1016/j.cortex.2019.11.003.
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Bula, German. "Passions, consciousness, and the Rosetta Stone: Spinoza and embodied, extended, and affective cognition." Adaptive Behavior 27, no. 1 (2018): 7–15. http://dx.doi.org/10.1177/1059712318790739.
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Baruch Spinoza is often cited as a forerunner of current ideas in neuroscience and neurobiology and is seen as an early champion of embodied cognition. This article aims to specify in what way Spinoza’s ideas are useful to current research on the mind-body problem. Rather than seeking coincidences here and there between Spinoza’s positions and current findings, the article proposes that Spinoza provides a broad ontological framework that can guide research. This idea is fleshed out by contrasting Spinoza’s ideas on emotions, the treatment of harmful passions, and the mind-body relationship with those of Descartes; by showing how Spinoza’s positions are importantly different from those of current neuroscience; and by showing how Spinoza proposes a solution to the problem of consciousness that makes use of his ontological framework, which suggests an heuristic in which mind and body can be treated as hermeneutical keys to each other.
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Music, Graham. "Babies and bathwaters: attachment, neuroscience, evolution and the left." Soundings 73, no. 73 (2019): 111–28. http://dx.doi.org/10.3898/soun.73.09.2019.
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This article challenges thinkers and activists on the left who are over-suspicious of ideas heralding from disciplines such as interpersonal neurobiology, attachment theory, developmental psychology, and perhaps especially, evolutionary theory. Although scepticism is frequently warranted, especially as such discourses are often co-opted for neoliberal or far right ends, there is much in all of them that melds well with critiques of hegemonic social orders, providing potential fuel for those working for social change. Much work, for example that of Amy Cuddy, can be interpreted both conservatively and progressively. Work from within an attachment theory paradigm can play a crucial part in the battle of ideas: it has a huge amount to teach about how to create a more humane and egalitarian world, and in countering neoliberal beliefs that humans are innately primarily aggressive, competitive or selfish, or have selfish genes. The days are now over when the biological, psychological and the social need to be pitted against each other. Rather, they now have to be seen as mutually constituted. The brain is a social organ, embedded, embodied, enactive and extended, in large part a reflection of the social conditions in which it grows.
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Lu, Kai, and David S. Vicario. "Toward a neurobiology of auditory object perception: What can we learn from the songbird forebrain?" Current Zoology 57, no. 6 (2011): 671–83. http://dx.doi.org/10.1093/czoolo/57.6.671.
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Abstract In the acoustic world, no sounds occur entirely in isolation; they always reach the ears in combination with other sounds. How any given sound is discriminated and perceived as an independent auditory object is a challenging question in neuroscience. Although our knowledge of neural processing in the auditory pathway has expanded over the years, no good theory exists to explain how perception of auditory objects is achieved. A growing body of evidence suggests that the selectivity of neurons in the auditory forebrain is under dynamic modulation, and this plasticity may contribute to auditory object perception. We propose that stimulus-specific adaptation in the auditory forebrain of the songbird (and perhaps in other systems) may play an important role in modulating sensitivity in a way that aids discrimination, and thus can potentially contribute to auditory object perception.
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Albert, Paul R., Chawki Benkelfat, and Laurent Descarries. "The neurobiology of depression—revisiting the serotonin hypothesis. I. Cellular and molecular mechanisms." Philosophical Transactions of the Royal Society B: Biological Sciences 367, no. 1601 (2012): 2378–81. http://dx.doi.org/10.1098/rstb.2012.0190.
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The serotonin (5-HT) hypothesis of depression dates from the 1960s. It originally postulated that a deficit in brain serotonin, corrected by antidepressant drugs, was the origin of the illness. Nowadays, it is generally accepted that recurring mood disorders are brain diseases resulting from the combination, to various degrees, of genetic and other biological as well as environmental factors, evolving through the lifespan. All areas of neuroscience, from genes to behaviour, molecules to mind, and experimental to clinical, are actively engaged in attempts at elucidating the pathophysiology of depression and the mechanisms underlying the efficacy of antidepressant treatments. This first of two special issues of Philosophical Transactions B seeks to provide an overview of current developments in the field, with an emphasis on cellular and molecular mechanisms, and how their unravelling opens new perspectives for future research.
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Dolmetsch, Ricardo. "Using iPS cells to study the underlying neurobiology of autism spectrum disorders and other neuro-developmental diseases." Neuroscience Research 71 (September 2011): e37-e38. http://dx.doi.org/10.1016/j.neures.2011.07.165.
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Jeromin, Andreas, Li-Lian Yuan, Andreas Frick, Paul Pfaffinger, and Daniel Johnston. "A Modified Sindbis Vector for Prolonged Gene Expression in Neurons." Journal of Neurophysiology 90, no. 4 (2003): 2741–45. http://dx.doi.org/10.1152/jn.00464.2003.
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Sindbis viruses have been widely used in neurobiology to express a variety of genes in cultured neurons, in cultured slices, and in vivo. They provide fast onset and high levels of expression of foreign genes, but the expression is limited to a short time window due to a shut-off of host protein synthesis. We have used a mutation in an essential gene (nsP2) of the life cycle of Sindbis, which allows the functional analysis of changes in protein expression for ≥6 days after infection. This Sindbis mutant (nsP2) was used to express enhanced green fluorescent protein (EGFP) in hippocampal neurons in culture and in vivo without any sign of toxicity, based on two-photon imaging and electrophysiology. In addition, the EGFP mutant virus can be injected in vivo to visualize spines and other details of neuronal structure. The Sindbis mutant described here provides an improved tool in neurobiology with reduced cytotoxicity and a prolonged time window of expression for novel applications in imaging and behavior. In addition, the use of this vector for the functional expression of mammalian voltage-gated ion channels in organotypic slices is demonstrated.
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Panksepp, Jaak. "Emotional feelings originate below the neocortex: Toward a neurobiology of the soul." Behavioral and Brain Sciences 30, no. 1 (2007): 101–3. http://dx.doi.org/10.1017/s0140525x07001094.
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Disregard of primary-process consciousness is endemic in mind science. Most neuroscientists subscribe to ruthless reductionism whereby mental qualities are discarded in preference for neuronal functions. Such ideas often lead to envisioning other animals, and all too often other humans, as unfeeling zombies. Merker correctly highlights how the roots of consciousness exist in ancient neural territories we share, remarkably homologously, with all the other vertebrates.
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Husemann, Jens, John D. Loike, Roman Anankov, Maria Febbraio, and Samuel C. Silverstein. "Scavenger receptors in neurobiology and neuropathology: Their role on microglia and other cells of the nervous system." Glia 40, no. 2 (2002): 195–205. http://dx.doi.org/10.1002/glia.10148.
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Faraone, Stephen V. "The pharmacology of amphetamine and methylphenidate: Relevance to the neurobiology of attention-deficit/hyperactivity disorder and other psychiatric comorbidities." Neuroscience & Biobehavioral Reviews 87 (April 2018): 255–70. http://dx.doi.org/10.1016/j.neubiorev.2018.02.001.
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Varley, Rosemary, and Michael Siegal. "Language, cognition, and the nature of modularity: Evidence from aphasia." Behavioral and Brain Sciences 25, no. 6 (2002): 702–3. http://dx.doi.org/10.1017/s0140525x02520124.
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We examine Carruthers’ proposal that sentences in logical form serve to create flexibility within central system modularity, enabling the combination of information from different modalities. We discuss evidence from aphasia and the neurobiology of input-output systems. This work suggests that there exists considerable capacity for interdomain cognitive processing without language mediation. Other challenges for a logical form account are noted.
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Adolphs, Ralph, and Daniel Andler. "Investigating Emotions as Functional States Distinct From Feelings." Emotion Review 10, no. 3 (2018): 191–201. http://dx.doi.org/10.1177/1754073918765662.
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We defend a functionalist approach to emotion that begins by focusing on emotions as central states with causal connections to behavior and to other cognitive states. The approach brackets the conscious experience of emotion, lists plausible features that emotions exhibit, and argues that alternative schemes (e.g., focusing on feelings or on neurobiology as the starting point) are unpromising candidates. We conclude with the benefits of our approach: one can study emotions in animals; one can look in the brain for the implementation of specific features; and one ends up with an architecture of the mind in which emotions are fully accommodated through their relations to the rest of cognition. Our article focuses on arguing for this general approach; as such, it is an essay in the philosophy of emotion rather than in the psychology or neuroscience of emotion.
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Okuda, Jiro. "Prospection or projection: Neurobiological basis of stimulus-independent mental traveling." Behavioral and Brain Sciences 30, no. 3 (2007): 328–29. http://dx.doi.org/10.1017/s0140525x07002142.
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AbstractThe number of studies concerning the neurobiology of human prospection is now rapidly exploding. Recent works suggest that prospection can be better understood in a broader context of self-projection into other times, places, or agents that can share the same cerebral basis involving medial aspects of prefrontal, parietal, and temporal cortices. Mental time travel may be extended more generally to “mental traveling,” accomplished by stimulus-independent mental processes typical of human thought.
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Pagel, Jim F. "Drug induced alterations in dreaming: An exploration of the dream data terrain outside activation-synthesis." Behavioral and Brain Sciences 27, no. 5 (2004): 702–7. http://dx.doi.org/10.1017/s0140525x04280165.
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Two meta-analyses of pharmacological research are presented, demonstrating that psychoactive drugs have consistent effects on EEG and sleep outside of their effects on REM sleep, and demonstrating that drugs other than those affecting sleep neurotransmitter systems and REM sleep can also alter reported nightmare occurrence. These data suggest that the neurobiology data terrain outside activation-synthesis may include sleep and dream electrophysiology, cognitive reports of dreaming, effects of alterations in consciousness on dreaming, immunology and host defense, and clinical therapies for sleep disorders.
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Bolker, Jessica A. "Selection of Models: Evolution and the Choice of Species for Translational Research." Brain, Behavior and Evolution 93, no. 2-3 (2019): 82–91. http://dx.doi.org/10.1159/000500317.
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Evolutionary thinking can inform the choice and assessment of model species in neuroscience, particularly when such models are intended to generate knowledge that will translate to humans. Avoiding errors that arise from oversimplified notions of phylogeny or genotype-phenotype mapping is one contribution; evolutionary biology also offers positive guidance. The challenge of finding adequate non-human models for translational research is particularly acute in neuroscience: neurobiological and behavioral phenotypes are complex and plastic, and many traits important in humans are absent, radically different, or difficult to assess in other species. Evolutionary perspectives help to articulate and address these challenges. Darwin’s description of “descent with modification” points to two aspects of evolution that can help us assess the matching between a prospective model species and its intended target. One is trees that represent the structure of phylogenetic relationships; the other is phenotypic traits, i.e. the unique characteristics of each species’ evolved biology and natural history. Mapping traits onto a phylogeny is the first step toward analyzing the source of similarities between a target and a potential model. Whether similar traits arise from shared ancestry or from adaptive convergence has important implications for what kinds of inferences can be justified, and for the likely translatability of findings. Evolution offers both a rich source of possible models, and guidance for choosing the best ones for a given purpose. Considering model choice from an evolutionary angle not only helps to answer the question “What species might be a good model for studying x?” but also suggests additional questions we should be asking to assess the utility of both potential and current models. Recognizing the diverse ways model organisms can function expands our search image as we seek species to study that can both extend general knowledge, and generate translatable insights relevant to human neurobiology and disease.
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Ijspeert, Auke J. "Amphibious and Sprawling Locomotion: From Biology to Robotics and Back." Annual Review of Control, Robotics, and Autonomous Systems 3, no. 1 (2020): 173–93. http://dx.doi.org/10.1146/annurev-control-091919-095731.
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A milestone in vertebrate evolution, the transition from water to land, owes its success to the development of a sprawling body plan that enabled an amphibious lifestyle. The body, originally adapted for swimming, evolved to benefit from limbs that enhanced its locomotion capabilities on submerged and dry ground. The first terrestrial animals used sprawling locomotion, a type of legged locomotion in which limbs extend laterally from the body (as opposed to erect locomotion, in which limbs extend vertically below the body). This type of locomotion—exhibited, for instance, by salamanders, lizards, and crocodiles—has been studied in a variety of fields, including neuroscience, biomechanics, evolution, and paleontology. Robotics can benefit from these studies to design amphibious robots capable of swimming and walking, with interesting applications in field robotics, in particular for search and rescue, inspection, and environmental monitoring. In return, robotics can provide useful scientific tools to test hypotheses in neuroscience, biomechanics, and paleontology. For instance, robots have been used to test hypotheses about the organization of neural circuits that can switch between swimming and walking under the control of simple modulation signals, as well as to identify the most likely gaits of extinct sprawling animals. Here, I review different aspects of amphibious and sprawling locomotion, namely gait characteristics, neurobiology, numerical models, and sprawling robots, and discuss fruitful interactions between robotics and other scientific fields.
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Patel, Y., J. Shin, P. A. Gowland, Z. Pausova, and T. Paus. "Maturation of the Human Cerebral Cortex During Adolescence: Myelin or Dendritic Arbor?" Cerebral Cortex 29, no. 8 (2018): 3351–62. http://dx.doi.org/10.1093/cercor/bhy204.
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Abstract Previous in vivo studies revealed robust age-related variations in structural properties of the human cerebral cortex during adolescence. Neurobiology underlying these maturational phenomena is largely unknown. Here we employ a virtual-histology approach to gain insights into processes associated with inter-regional variations in cortical microstructure and its maturation, as indexed by magnetization transfer ratio (MTR). Inter-regional variations in MTR correlate with inter-regional variations in expression of genes specific to pyramidal cells (CA1) and ependymal cells; enrichment analyses indicate involvement of these genes in dendritic growth. On the other hand, inter-regional variations in the change of MTR during adolescence correlate with inter-regional profiles of oligodendrocyte-specific gene expression. Complemented by a quantitative hypothetical model of the contribution of surfaces associated with dendritic arbor (1631 m2) and myelin (48 m2), these findings suggest that MTR signals are driven mainly by macromolecules associated with dendritic arbor while maturational changes in the MTR signal are associated with myelination.
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Alexander, L., and N. Farrelly. "Attending to adult ADHD: a review of the neurobiology behind adult ADHD." Irish Journal of Psychological Medicine 35, no. 3 (2017): 237–44. http://dx.doi.org/10.1017/ipm.2017.78.
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BackgroundAttention deficit hyperactivity disorder (ADHD) is a common disorder in childhood, which progresses to adulthood in about a fifth of cases. For various reasons, adult ADHD is a disorder not comprehensively assessed by psychiatrists, not least because the biological underpinnings are only recently being unmasked.AimsThis selective review targets psychiatrists without a background in neuroscience and aims to describe the neurobiological basis of ADHD.MethodsIn total, 40 articles from a PubMed search were selected for inclusion based on sample population and methodology (neuroimaging studies). Studies focussing on adult participants were selected preferentially for inclusion. Seminal articles relevant to childhood populations were included for the purpose of understanding general concepts around ADHD.ResultsThe neuropathology of ADHD is not rooted in a single anatomical area, but in multiple parallel and intersecting pathways, which have demonstrated impaired functional connectivity in ADHD brains. Dysfunction in executive function, reward processing, attention networks and default networks play major roles in the neuropathology of this condition. Biological findings vary between individuals, with some showing greater dysfunction at cortical levels and others at subcortical levels, which is in keeping with its clinical heterogeneity.ConclusionImproved symptomatology in adulthood is linked to a number of factors. Maturation of the prefrontal cortex in early adulthood contributes to symptom attenuation in many cases, meaning that individuals with cortical dysfunction are more likely to grow out of symptoms, whereas individuals with subcortical dysfunction may be less likely to do so. There is emerging evidence for a similar but distinct disorder arising de novo in adulthood.
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Ferrari, Pier F. "The neuroscience of social relations. A comparative-based approach to empathy and to the capacity of evaluating others’ action value." Behaviour 151, no. 2-3 (2014): 297–313. http://dx.doi.org/10.1163/1568539x-00003152.
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One of the key questions in understanding human morality is how central are emotions in influencing our decisions and in our moral judgments. Theoretical work has proposed that empathy could play an important role in guiding our tendencies to behave altruistically or selfishly. Neurosciences suggest that one of the core elements of empathic behaviour in human and nonhuman primates is the capacity to internally mimic the behaviour of others, through the activation of shared motor representations. Part of the neural circuits involves parietal and premotor cortical regions (mirror system), in conjunction with other areas, such as the insula and the anterior cingulate cortex. Together with this embodied neural mechanism, there is a cognitive route in which individuals can evaluate the social situation without necessary sharing the emotional state of others. For example, several brain areas of the prefrontal cortex track the effects of one’s own behaviour and of the value of one’s own actions in social contexts. It is here proposed that, moral cognition could emerge as the consequence of the activity of emotional processing brain networks, probably involving mirror mechanisms, and of brain regions that, through abstract-inferential processing, evaluate the social context and the value of actions in terms of abstract representations. A comparative-based approach to the neurobiology of social relations and decision-making may explain how complex mental faculties, such as moral judgments, have their foundations in brain networks endowed with functions related to emotional and abstract-evaluation processing of goods. It is proposed that in primate evolution these brain circuits have been co-opted in the social domain to integrate mechanisms of self-reward, estimation of negative outcomes, with emotional engagement.
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Jones, Wendy, Ursula Bellugi, Zona Lai, et al. "II. Hypersociability in Williams Syndrome." Journal of Cognitive Neuroscience 12, supplement 1 (2000): 30–46. http://dx.doi.org/10.1162/089892900561968.
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Studies of abnormal populations provide a rare opportunity for examining relationships between cognition, genotype and brain neurobiology, permitting comparisons across these different levels of analysis. In our studies, we investigate individuals with a rare, genetically based disorder called Williams syndrome (WMS) to draw links among these levels. A critical component of such a cross-domain undertaking is the clear delineation of the phenotype of the disorder in question. Of special interest in this paper is a relatively unexplored unusual social phenotype in WMS that includes an overfriendly and engaging personality. Four studies measuring distinct aspects of hypersocial behavior in WMS are presented, each probing specific aspects in WMS infants, toddlers, school age children, and adults. The abnormal profile of excessively social behavior represents an important component of the phenotype that may distinguish WMS from other developmental disorders. Furthermore, the studies show that the profile is observed across a wide range of ages, and emerges consistently across multiple experimental paradigms. These studies of hypersocial behavior in WMS promise to provide the ground-work for crossdisciplinary analyses of gene-brain-behavior relationships.
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Herculano-Houzel, Suzana, Kenneth Catania, Paul R. Manger, and Jon H. Kaas. "Mammalian Brains Are Made of These: A Dataset of the Numbers and Densities of Neuronal and Nonneuronal Cells in the Brain of Glires, Primates, Scandentia, Eulipotyphlans, Afrotherians and Artiodactyls, and Their Relationship with Body Mass." Brain, Behavior and Evolution 86, no. 3-4 (2015): 145–63. http://dx.doi.org/10.1159/000437413.
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Comparative studies amongst extant species are one of the pillars of evolutionary neurobiology. In the 20th century, most comparative studies remained restricted to analyses of brain structure volume and surface areas, besides estimates of neuronal density largely limited to the cerebral cortex. Over the last 10 years, we have amassed data on the numbers of neurons and other cells that compose the entirety of the brain (subdivided into cerebral cortex, cerebellum, and rest of brain) of 39 mammalian species spread over 6 clades, as well as their densities. Here we provide that entire dataset in a format that is readily useful to researchers of any area of interest in the hope that it will foster the advancement of evolutionary and comparative studies well beyond the scope of neuroscience itself. We also reexamine the relationship between numbers of neurons, neuronal densities and body mass, and find that in the rest of brain, but not in the cerebral cortex or cerebellum, there is a single scaling rule that applies to average neuronal cell size, which increases with the linear dimension of the body, even though there is no single scaling rule that relates the number of neurons in the rest of brain to body mass. Thus, larger bodies do not uniformly come with more neurons - but they do fairly uniformly come with larger neurons in the rest of brain, which contains a number of structures directly connected to sources or targets in the body.
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Masters, Roger D., and Myron J. Coplan. "A dynamic, multifactorial model of alcohol, drug abuse, and crime: linking neuroscience and behavior to toxicology." Social Science Information 38, no. 4 (1999): 591–624. http://dx.doi.org/10.1177/053901899038004005.
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Although there is increasing recognition that many dysfunctional behaviors and diseases require multifactorial explanations that integrate biological and socio-cultural variables, such an approach requires fundamental conceptual changes. To explain geographical and temporal variations in alcohol and drug abuse and in criminal behavior, we propose a dynamic, multifactorial model that integrates findings in neurobiology and social science with toxicology. This model is based on a sequence of probabilistic relationships. (1) Some individuals are potential alcoholics or drug addicts for genetic or developmental reasons that may also be associated with attention deficit hyperactivity disorder (ADHD), antisocial personality, or other traits that have been linked to criminal behavior. (2) Uptake of lead, manganese, and other neurotoxic substances from the environment can downregulate dopamine, glutamate, serotonin, and other neurotransmitters necessary for learning and normal impulse control. (3) Uptake of lead and other neurotoxins is increased by dietary deficits in calcium, zinc, and iron which in turn are associated with poverty, stress, and lactose intolerance. (4) Additional environmental factors, such as silicofluoride use in treatment of public water supplies, also increase uptake of lead. (5) Fetal and childhood uptake of lead and other toxins is associated with both developmental and learning deficits and with continued neurotoxicity during teenage and young adult years. (6) Alcohol and drug abuse can function as crude self-medication to compensate for downregulation of serotonin, dopamine and other affected neurotransmitters. (7) Lead neurotoxicity increases the market for alcohol and hence the total number of active alcoholics. (8) This increase in a community's market size reflects prolonged recruitment of potential alcohol users (higher average age of first use of alcohol is correlated to size of market for alcohol). (9) Larger markets for alcohol lead to larger markets for cocaine and crack. (10) These linked markets are a key factor in different rates of crime, since higher average age of first use of alcohol, of cocaine, or of crack is associated with a higher rate of crime and more criminals who were using cocaine or crack at the time of their offense. When otherwise unexplained geographical and historical differences in rates of crime are analyzed from this perspective, environmental pollution and the use of silicofluorides in water treatment seem to play a critical role in triggering social dysfunction. This dynamic, multifactorial approach may provide a model for studying the epidemiology of other dysfunctional behaviors and diseases, such as ADD/ADHD, asthma, Parkinson's disease, and Alzheimer's disease, which have been traced to varied combinations of genetic vulnerabilities, toxic metals, developmental insults, and social stresses.
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Takahashi, Hidehiko, Makiko Yamada, and Tetsuya Suhara. "Functional Significance of Central D1 Receptors in Cognition: Beyond Working Memory." Journal of Cerebral Blood Flow & Metabolism 32, no. 7 (2012): 1248–58. http://dx.doi.org/10.1038/jcbfm.2011.194.
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The role of dopamine D1 receptors in prefrontal cortex function, including working memory, is well acknowledged. However, relatively little is known about their role in other cognitive or emotional functions. We measured both D1 and D2 receptors in the brain using positron emission tomography in healthy subjects, with the aim of elucidating how regional D1 and D2 receptors are differentially involved in cognitive and emotional functions beyond working memory. We found an inverted U-shaped relation between prefrontal D1 receptor availability and Wisconsin Card Sorting Test performance, indicating that too little or too much D1 receptor stimulation impairs working memory or set shifting. In addition, variability of D1 receptor availability in the amygdala and striatum was related to individual differences in emotional responses and decision-making processes, respectively. These observations suggest that the variability of available D1 receptors might be associated with individual differences in brain functions that require phasic dopamine release. An interdisciplinary approach combining molecular imaging of dopamine neurotransmission with cognitive neuroscience and clinical psychiatry will provide new perspectives for understanding the neurobiology of neuropsychiatric disorders such as schizophrenia, addiction and Parkinson's disease, as well as novel therapeutics for cognitive impairments observed in them.
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Killackey, Herbert P. "Neocortical Expansion: An Attempt toward Relating Phylogeny and Ontogeny." Journal of Cognitive Neuroscience 2, no. 1 (1990): 1–17. http://dx.doi.org/10.1162/jocn.1990.2.1.1.
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The neocortex is the most characteristic feature of the human brain. On gross inspection, its convoluted surfaces can be seen to have overgrown and covered most other brain structures. In the functional sphere, it is to the neocortex that we attribute those behaviors assumed to be most uniquely human such as cognition and linguistic behavior. This essay is an attempt to understand how this structure expanded during the course of mammalian evolution. At present, any attempt must be more speculative than definitive, but it is offered in the hope that it will generate more discussion on a topic that is central to all neurobiology, as well as a number of allied disciplines. I will proceed by outlining current views on the evolution of the brain, briefly review the organization of the somatosensory cortex in several mammalian forms, and then discuss in some detail ontogenetic mechanisms that may have some bearing on neocortical phylogeny. The primary proposition put forth is that the mammalian neocortex is relatively unspecified by strict genetic means, and that this allowed the neocortex to expand and adapt to a variety of circumstances during the course of phylogeny.
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Healy-Stoffel, Michelle, and Beth Levant. "N-3 (Omega-3) Fatty Acids: Effects on Brain Dopamine Systems and Potential Role in the Etiology and Treatment of Neuropsychiatric Disorders." CNS & Neurological Disorders - Drug Targets 17, no. 3 (2018): 216–32. http://dx.doi.org/10.2174/1871527317666180412153612.
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Background & Objective: A number of neuropsychiatric disorders, including Parkinson's disease, schizophrenia, attention deficit hyperactivity disorder, and, to some extent, depression, involve dysregulation of the brain dopamine systems. The etiology of these diseases is multifactorial, involving genetic and environmental factors. Evidence suggests that inadequate levels of n-3 (omega- 3) polyunsaturated fatty acids (PUFA) in the brain may represent a risk factor for these disorders. These fatty acids, which are derived from the diet, are a major component of neuronal membranes and are of particular importance in brain development and function. Low levels of n-3 PUFAs in the brain affect the brain dopamine systems and, when combined with appropriate genetic and other factors, increase the risk of developing these disorders and/or the severity of the disease. This article reviews the neurobiology of n-3 PUFAs and their effects on dopaminergic function. Conclusion: Clinical studies supporting their role in the etiologies of diseases involving the brain dopamine systems and the potential of n-3 PUFAs in the treatment of these disorders are discussed.
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Mathias, Samuel R., Emma E. M. Knowles, Josephine Mollon, et al. "Minimal Relationship between Local Gyrification and General Cognitive Ability in Humans." Cerebral Cortex 30, no. 6 (2020): 3439–50. http://dx.doi.org/10.1093/cercor/bhz319.
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Abstract Previous studies suggest that gyrification is associated with superior cognitive abilities in humans, but the strength of this relationship remains unclear. Here, in two samples of related individuals (total N = 2882), we calculated an index of local gyrification (LGI) at thousands of cortical surface points using structural brain images and an index of general cognitive ability (g) using performance on cognitive tests. Replicating previous studies, we found that phenotypic and genetic LGI–g correlations were positive and statistically significant in many cortical regions. However, all LGI–g correlations in both samples were extremely weak, regardless of whether they were significant or nonsignificant. For example, the median phenotypic LGI–g correlation was 0.05 in one sample and 0.10 in the other. These correlations were even weaker after adjusting for confounding neuroanatomical variables (intracranial volume and local cortical surface area). Furthermore, when all LGIs were considered together, at least 89% of the phenotypic variance of g remained unaccounted for. We conclude that the association between LGI and g is too weak to have profound implications for our understanding of the neurobiology of intelligence. This study highlights potential issues when focusing heavily on statistical significance rather than effect sizes in large-scale observational neuroimaging studies.
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Derazshamshir, Ali, Süleyman Aşır, Ilgım Göktürk, Sisem Ektirici, Fatma Yılmaz, and Adil Denizli. "Polymethacryloyl-L-Phenylalanine [PMAPA]-Based Monolithic Column for Capillary Electrochromatography." Journal of Chromatographic Science 57, no. 8 (2019): 758–65. http://dx.doi.org/10.1093/chromsci/bmz047.
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Abstract The ability to detect catecholamines (CAs) and their metabolites is vital to understand the mechanism behind the neuronal diseases. Neurochemistry aims to provide an improved pharmacological, molecular and physiological understanding of complex brain chemistries by analytical techniques. Capillary electrophoresis (CE) is one such analytical technique that enables the study of various chemical species ranging from amino acids and peptides to natural products and drugs. CE can easily adapt the changes in research focus and in recent years remains an applicable technique for investigating neuroscience and single cell neurobiology. The prepared phenylalanine-based hydrophobic monolithic column, Polymethacryloyl-L-phenylalanine [PMAPA], was used as a stationary phase in capillary electrochromatography to separate CAs that are similar in size and shape to each other including dopamine (DA) and norepinephrine (NE) via hydrophobic interactions. Separation carried out in a short period of 17 min was performed with the electrophoretic mobility of 5.54 × 10−6 m2 V−1 s−1 and 7.60 × 10−6 m2 V−1 s−1 for DA and NE, respectively, at pH 7.0, 65% acetonitrile ratio with 100 mbar applied pressure by the developed hydrophobic monolithic column without needing any extra process such as imprinting or spacer arms to immobilize ligands used in separation.
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Tay, Jonathan, Robin G. Morris, and Hugh S. Markus. "Apathy after stroke: Diagnosis, mechanisms, consequences, and treatment." International Journal of Stroke 16, no. 5 (2021): 510–18. http://dx.doi.org/10.1177/1747493021990906.
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Apathy is a reduction in goal-directed activity in the cognitive, behavioral, emotional, or social domains of a patient’s life and occurs in one out of three patients after stroke. Despite this, apathy is clinically under-recognized and poorly understood. This overview provides a contemporary introduction to apathy in stroke for researchers and practitioners, covering topics including diagnosis, neurobiological mechanisms, associated consequences, and potential treatments for apathy. Apathy is often misdiagnosed as other post-stroke conditions such as depression. Accurate differential diagnosis of apathy, which manifests as reductions in initiative, and depression, which manifests as negative emotionality, is important as it informs prognosis. Research on the neurobiology of apathy suggests that there are few consistent associations between stroke lesion location and the development of apathy. These may be resolved by adopting a network neuroscience approach, which models apathy as a pathology arising from structural or functional damage to brain networks underlying motivated behavior. Importantly, networks can be affected by physiological changes related to stroke, including the acute infarct but also diaschisis and neurodegeneration. Aside from neurobiological changes, apathy is also associated with other negative outcome measures such as functional disability, cognitive impairment, and emotional distress, suggesting that apathy is indicative of a worse prognosis following stroke. Unfortunately, high-quality trials aimed at treating apathy are scarce. Antidepressants may have limited effects on apathy. Acetylcholine and dopamine pharmacotherapy, behavioral interventions, and transcranial magnetic stimulation may be more promising avenues for treatment.
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Machin, A. J., and R. I. M. Dunbar. "The brain opioid theory of social attachment: a review of the evidence." Behaviour 148, no. 9-10 (2011): 985–1025. http://dx.doi.org/10.1163/000579511x596624.
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AbstractThe psychology of close human relationships is increasingly well understood and our understanding of the neurobiology of the onset of pairbonding behaviour in a range of species has benefited from the use of rodent-based models. However, the human literature has suffered from a lack of focus upon the unique nature of primate social bonds and has so far failed to adequately identify the neurobiological and behavioural mechanisms which maintain these complex, diverse and enduring social networks. One neurobiological mechanism that has been overlooked is the endogenous opioid system. Though less explicitly researched than the more familiar oxytocin/vasopressin system, there is considerable evidence that the opioids play a fundamental role in sociality, especially in the primates. This review summarises our current understanding of the evidence for the role of this system in prosocial behaviour in non-primate mammals, nonhuman primates and humans. An important conclusion is that the opioid system may play a more central role in sociality in primates (including humans) than in other mammalian taxa.
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Costanza, Alessandra, Andrea Amerio, Andrea Aguglia, et al. "When Sick Brain and Hopelessness Meet: Some Aspects of Suicidality in the Neurological Patient." CNS & Neurological Disorders - Drug Targets 19, no. 4 (2020): 257–63. http://dx.doi.org/10.2174/1871527319666200611130804.
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: Neurological diseases expose individuals to a higher risk of suicidal ideation and suicidal behavior, including completed suicides and suicide attempts. They also represent a paradigmatic arena to study the etiopathogenic mechanisms underlying suicidality because they are emblematic of the heterogeneity and complexity of mutual interrelationships characterizing this issue. On the one hand, neurological diseases imply strictly biological impairments that are postulated to be the basis of vulnerability to suicide or result in the need for treatments for which a suicidal risk has been hypothesized. On the other hand, they question some subjective experiences of neurological patients, up to near existential positions. Often, in fact, they are accompanied by severe hopelessness. The latter may originate in, particularly for the most severe neurological diseases, the absence of curative treatments, unpredictable disease progression that leads to acute relapses or chronicity, a decrease in autonomy or selfidentity, progressive social isolation, a sense of becoming useless, and perception of feeling stigmatized. This may ultimately cause a slip into experiencing an absurd condition. At the confluence of neurobiology and hopelessness, frequent psychiatric comorbidities may play a primary role. To conclude, neurological patients require special attention from clinicians in form of openly verbalizing and exploring the suicidal thematic, inquiring about protective and risk factors, and promptly initiating both a psychopharmacological treatment and, where possible, psychological support.
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Schmitt, J. Eric, Armin Raznahan, Siyuan Liu, and Michael C. Neale. "The Heritability of Cortical Folding: Evidence from the Human Connectome Project." Cerebral Cortex 31, no. 1 (2020): 702–15. http://dx.doi.org/10.1093/cercor/bhaa254.
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Abstract The mechanisms underlying cortical folding are incompletely understood. Prior studies have suggested that individual differences in sulcal depth are genetically mediated, with deeper and ontologically older sulci more heritable than others. In this study, we examine FreeSurfer-derived estimates of average convexity and mean curvature as proxy measures of cortical folding patterns using a large (N = 1096) genetically informative young adult subsample of the Human Connectome Project. Both measures were significantly heritable near major sulci and primary fissures, where approximately half of individual differences could be attributed to genetic factors. Genetic influences near higher order gyri and sulci were substantially lower and largely nonsignificant. Spatial permutation analysis found that heritability patterns were significantly anticorrelated to maps of evolutionary and neurodevelopmental expansion. We also found strong phenotypic correlations between average convexity, curvature, and several common surface metrics (cortical thickness, surface area, and cortical myelination). However, quantitative genetic models suggest that correlations between these metrics are largely driven by nongenetic factors. These findings not only further our understanding of the neurobiology of gyrification, but have pragmatic implications for the interpretation of heritability maps based on automated surface-based measurements.
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Pérez-Valenzuela, Catherine, Gonzalo Terreros, and Alexies Dagnino-Subiabre. "Effects of stress on the auditory system: an approach to study a common origin for mood disorders and dementia." Reviews in the Neurosciences 30, no. 3 (2019): 317–24. http://dx.doi.org/10.1515/revneuro-2018-0018.
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Abstract The concept of stress is a fundamental piece to understand how organisms can adapt to the demands produced by a continuously changing environment. However, modern lifestyle subjects humans to high levels of negative stress or distress, which increases the prevalence of mental illnesses. Definitely, stress has become the pandemic of the 21st century, a fact that demands a great intellectual effort from scientists to understand the neurobiology of stress. This review proposes an innovative point of view to understand that mood disorders and dementia have a common etiology in a stressful environment. We propose that distress produces sensory deprivation, and this interferes with the connection between the brain and the environment in which the subject lives. The auditory system can serve as an example to understand this idea. In this sense, distress impairs the auditory system and induces hearing loss or presbycusis at an early age; this can increase the cognitive load in stressed people, which can stimulate the development of dementia in them. On the other hand, distress impairs the auditory system and increases the excitability of the amygdala, a limbic structure involved in the emotional processing of sounds. A consequence of these alterations could be the increase in the persistence of auditory fear memory, which could increase the development of mood disorders. Finally, it is important to emphasize that stress is an evolutionary issue that is necessary to understand the mental health of humans in these modern times. This article is a contribution to this discussion and will provide insights into the origin of stress-related neuropsychiatric disorders.
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Borelli, Wyllians Vendramini, Karoline Carvalho Carmona, Adalberto Studart-Neto, Ricardo Nitrini, Paulo Caramelli, and Jaderson Costa da Costa. "Operationalized definition of older adults with high cognitive performance." Dementia & Neuropsychologia 12, no. 3 (2018): 221–27. http://dx.doi.org/10.1590/1980-57642018dn12-030001.
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ABSTRACT Recently, there has been an increasing number of studies on exceptional cognitive aging. Herein, we aim to objectively provide the operationalized characterization of older adults with unusually high memory ability. Some authors have defined them as “SuperAgers”, individuals aged 80 years or older with memory ability similar or superior to middle-aged subjects. On the other hand, the terminology “high-performing older adults” (HPOA) seems to appropriately conceptualize these individuals without exaggeration. A threshold for age is not a reliable criterion, but may be defined as 75 and 80 years of age for developing and developed countries, respectively. We propose that HPOA may exhibit episodic memory test scores equal to or greater than those of individuals aged 50-60 years, according to the validated tables for the respective country. This group must also have global cognition scores within expected average values for age and education. Executive functioning may play a central role in the exceptional memory performance of this group. Further studies are essential to confirm existing findings and may provide important evidence for cognitive aging theory and the neurobiology of dementia.
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Patel, Aniruddh D. "Vocal learning as a preadaptation for the evolution of human beat perception and synchronization." Philosophical Transactions of the Royal Society B: Biological Sciences 376, no. 1835 (2021): 20200326. http://dx.doi.org/10.1098/rstb.2020.0326.
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The human capacity to synchronize movements to an auditory beat is central to musical behaviour and to debates over the evolution of human musicality. Have humans evolved any neural specializations for music processing, or does music rely entirely on brain circuits that evolved for other reasons? The vocal learning and rhythmic synchronization hypothesis proposes that our ability to move in time with an auditory beat in a precise, predictive and tempo-flexible manner originated in the neural circuitry for complex vocal learning. In the 15 years since the hypothesis was proposed a variety of studies have supported it. However, one study has provided a significant challenge to the hypothesis. Furthermore, it is increasingly clear that vocal learning is not a binary trait animals have or lack, but varies more continuously across species. In the light of these developments and of recent progress in the neurobiology of beat processing and of vocal learning, the current paper revises the vocal learning hypothesis. It argues that an advanced form of vocal learning acts as a preadaptation for sporadic beat perception and synchronization (BPS), providing intrinsic rewards for predicting the temporal structure of complex acoustic sequences. It further proposes that in humans, mechanisms of gene-culture coevolution transformed this preadaptation into a genuine neural adaptation for sustained BPS. The larger significance of this proposal is that it outlines a hypothesis of cognitive gene-culture coevolution which makes testable predictions for neuroscience, cross-species studies and genetics. This article is part of the theme issue ‘Synchrony and rhythm interaction: from the brain to behavioural ecology’.
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van der Meer, Dennis, Jaroslav Rokicki, Tobias Kaufmann, et al. "Brain scans from 21,297 individuals reveal the genetic architecture of hippocampal subfield volumes." Molecular Psychiatry 25, no. 11 (2018): 3053–65. http://dx.doi.org/10.1038/s41380-018-0262-7.
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Abstract The hippocampus is a heterogeneous structure, comprising histologically distinguishable subfields. These subfields are differentially involved in memory consolidation, spatial navigation and pattern separation, complex functions often impaired in individuals with brain disorders characterized by reduced hippocampal volume, including Alzheimer’s disease (AD) and schizophrenia. Given the structural and functional heterogeneity of the hippocampal formation, we sought to characterize the subfields’ genetic architecture. T1-weighted brain scans (n = 21,297, 16 cohorts) were processed with the hippocampal subfields algorithm in FreeSurfer v6.0. We ran a genome-wide association analysis on each subfield, co-varying for whole hippocampal volume. We further calculated the single-nucleotide polymorphism (SNP)-based heritability of 12 subfields, as well as their genetic correlation with each other, with other structural brain features and with AD and schizophrenia. All outcome measures were corrected for age, sex and intracranial volume. We found 15 unique genome-wide significant loci across six subfields, of which eight had not been previously linked to the hippocampus. Top SNPs were mapped to genes associated with neuronal differentiation, locomotor behaviour, schizophrenia and AD. The volumes of all the subfields were estimated to be heritable (h2 from 0.14 to 0.27, all p < 1 × 10–16) and clustered together based on their genetic correlations compared with other structural brain features. There was also evidence of genetic overlap of subicular subfield volumes with schizophrenia. We conclude that hippocampal subfields have partly distinct genetic determinants associated with specific biological processes and traits. Taking into account this specificity may increase our understanding of hippocampal neurobiology and associated pathologies.
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Leslie, John B., and W. David Watkins. "Eicosanoids in the central nervous system." Journal of Neurosurgery 63, no. 5 (1985): 659–68. http://dx.doi.org/10.3171/jns.1985.63.5.0659.
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✓ All mammalian tissue investigated to date is capable of eicosanoid biosynthesis in response to various activating stimuli. While the importance of these metabolites as major mediators of many normal physiological processes and some pathophysiological conditions has not been proven, it is evident that these compounds are at least important modulators of many cellular and organ system functions. This review is intended to provide the reader with a brief overview of eicosanoid biology, with specific reference to the neurosciences. The increasing knowledge about the role of the eicosanoids in neurobiology may contribute to the understanding and treatment of many neurological diseases. The eicosanoids comprise several groups of biologically active unsaturated fatty acids: the “primary” prostaglandins, the cyclic endoperoxides, the prostanoids, the leukotrienes, and other acid lipids. This article includes a review of the enzymatic pathways of biosynthesis and metabolism of eicosanoids in man, and the pertinent structural nomenclature. The general basic and clinical pharmacological effects of the more important compounds on vascular perfusion, platelet function, intracellular enzyme activity, and interactions with other mediators of cellular activity are reviewed. A more detailed review of the actions of eicosanoids as mediators or modifiers of central nervous system physiology and pathophysiology is presented. Recent animal and human studies on the use and alterations of the eicosanoid metabolites is summarized, specifically where they relate to several clinical problem areas of interest to the neurosurgeon and neurobiologist. These areas include cerebrovascular circulation physiology, cerebral ischemia, cerebral vasospasm following subarachnoid hemor-rhage, migraine headaches, hypothalamic function, neurotransmission, and nociception. A bibliography of 92 articles for further review is also included.
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Gu, Jianguo, Min Zhuo, Michael Caterina, et al. "Molecular Pain, a New Era of Pain Research and Medicine." Molecular Pain 1 (January 1, 2005): 1744–8069. http://dx.doi.org/10.1186/1744-8069-1-1.
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Molecular pain is a relatively new and rapidly expanding research field that represents an advanced step from conventional pain research. Molecular pain research addresses physiological and pathological pain at the cellular, subcellular and molecular levels. These studies integrate pain research with molecular biology, genomics, proteomics, modern electrophysiology and neurobiology. The field of molecular pain research has been rapidly expanding in the recent years, and has great promise for the identification of highly specific and effective targets for the treatment of intractable pain. Although several existing journals publish articles on classical pain research, none are specifically dedicated to molecular pain research. Therefore, a new journal focused on molecular pain research is needed. Molecular Pain, an Open Access, peer-reviewed, online journal, will provide a forum for molecular pain scientists to communicate their research findings in a targeted manner to others in this important and growing field.
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Fields, R. Douglas, and Philip Lee. "A Look Inside." Neuron Glia Biology 1, no. 2 (2004): 95–96. http://dx.doi.org/10.1017/s1740925x04000298.
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Standard neurobiology textbooks commonly do not contain a chapter on cancer, and the word might not even appear in the index. Its absence cannot be explained simply on the grounds that the subject falls more appropriately within the clinical realm, because you will find chapters devoted to various other nervous system diseases. Could this intellectual blind spot result from the fact that mature neurons, being post-mitotic, do not succumb to the disease? This absence in most texts is curious, considering the severe functional implications. The word is sometimes used metaphorically to connote an unstoppable process of destruction, and indeed some forms of brain cancer present the most dire prognosis of any cancer. But more importantly the neglect of this subject is curious, because on a molecular and cellular level, cancer is the result of biological processes that are at the forefront of modern neurobiological research. These include such current hot-topic areas as intraand inter-cellular signaling networks, regulation of gene transcription, control of cellular differentiation, regulation of cell motility, migration and cell death; the secretion and response to growth factors, and interactions with the vascular and immune systems. Finally, the current enthusiasm and promising research on the use of stem cells for therapeutic treatment of nervous system disease has brought us face-to-face with our ignorance in this area, as we find that many types of stem cells transplanted into the brain form tumors. This issue of Neuron Glia Biology contains a special collection of original research papers on cancer in the peripheral and central nervous system and a review on the subject. These papers are introduced below by Special Feature Editor, Philip Lee.
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Klyushnikov, Sergey A. "Huntington’s disease." L.O. Badalyan Neurological Journal 1, no. 3 (2020): 139–58. http://dx.doi.org/10.17816/2686-8997-2020-1-3-139-158.
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Huntingtons disease is one of the most common hereditary neurodegenerative diseases, which remains practically incurable, inevitably leading to the disability of patients and premature death. A fairly wide prevalence in the world, the special severity of the course, the almost complete penetrance of the mutant gene, the peculiarity of clinical and genetic correlations in Huntingtons disease have attracted researchers specializing in neuroscience for many years. The study of the molecular neurobiology of Huntingtons disease over the past decades has largely contributed to significant progress in molecular biology, genetics, and many other biomedical disciplines. At the same time, Huntingtons disease has become a model disease in resolving issues of genetic counseling and prognostic testing in modern medical genetics. The review provides brief facts on the history of the study of the disease, including mapping and identification of the mutant gene. The issues of etiology and pathogenesis, molecular genetics of the disease, epidemiology, diagnostics, and differential diagnostics are discussed in detail. The spectrum of clinical manifestations of Huntingtons disease, its various forms, and course features are presented. From a modern perspective, the problem of developing valid biomarkers of both the manifest and the asymptomatic stages of the disease, as well as the course of the pathological process, are highlighted. The main issues of primary and secondary prevention of Huntingtons disease, bioethical principles of conducting genetic counseling for families burdened by this disease are outlined. The approaches to the symptomatic treatment of Huntingtons disease are described, a review of the main promising experimental therapeutic methods that can potentially slow down or stop the progression of the disease, as well as prevent its manifestation in asymptomatic carriers of the mutant gene, are presented. An important contribution of patient organizations to addressing issues affecting the interests of burdened families, scientific and clinical research on the disease was noted. Literature was searched and analyzed using the databases of Scopus, Web of Science, Pubmed (MedLine), eLibrary.
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Smith, D. J., V. Escott-Price, G. Davies, et al. "Genome-wide analysis of over 106 000 individuals identifies 9 neuroticism-associated loci." Molecular Psychiatry 21, no. 6 (2016): 749–57. http://dx.doi.org/10.1038/mp.2016.49.
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Abstract Neuroticism is a personality trait of fundamental importance for psychological well-being and public health. It is strongly associated with major depressive disorder (MDD) and several other psychiatric conditions. Although neuroticism is heritable, attempts to identify the alleles involved in previous studies have been limited by relatively small sample sizes. Here we report a combined meta-analysis of genome-wide association study (GWAS) of neuroticism that includes 91 370 participants from the UK Biobank cohort, 6659 participants from the Generation Scotland: Scottish Family Health Study (GS:SFHS) and 8687 participants from a QIMR (Queensland Institute of Medical Research) Berghofer Medical Research Institute (QIMR) cohort. All participants were assessed using the same neuroticism instrument, the Eysenck Personality Questionnaire-Revised (EPQ-R-S) Short Form’s Neuroticism scale. We found a single-nucleotide polymorphism-based heritability estimate for neuroticism of ∼15% (s.e.=0.7%). Meta-analysis identified nine novel loci associated with neuroticism. The strongest evidence for association was at a locus on chromosome 8 (P=1.5 × 10−15) spanning 4 Mb and containing at least 36 genes. Other associated loci included interesting candidate genes on chromosome 1 (GRIK3 (glutamate receptor ionotropic kainate 3)), chromosome 4 (KLHL2 (Kelch-like protein 2)), chromosome 17 (CRHR1 (corticotropin-releasing hormone receptor 1) and MAPT (microtubule-associated protein Tau)) and on chromosome 18 (CELF4 (CUGBP elav-like family member 4)). We found no evidence for genetic differences in the common allelic architecture of neuroticism by sex. By comparing our findings with those of the Psychiatric Genetics Consortia, we identified a strong genetic correlation between neuroticism and MDD and a less strong but significant genetic correlation with schizophrenia, although not with bipolar disorder. Polygenic risk scores derived from the primary UK Biobank sample captured ∼1% of the variance in neuroticism in the GS:SFHS and QIMR samples, although most of the genome-wide significant alleles identified within a UK Biobank-only GWAS of neuroticism were not independently replicated within these cohorts. The identification of nine novel neuroticism-associated loci will drive forward future work on the neurobiology of neuroticism and related phenotypes.
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Price, Jack, Alcino J. Silva, Steven A. Kushner, et al. "Neurobiology." Current Opinion in Neurobiology 12, no. 1 (2002): 1–7. http://dx.doi.org/10.1016/s0959-4388(02)00282-9.
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