Neuroscientist最新文献

Brain plasticity is the ability of the nervous system to change its structure and functioning in response to experiences. These changes occur mainly at synaptic connections, and this plasticity is named synaptic plasticity. During postnatal development, environmental influences trigger changes in synaptic plasticity that will play a crucial role in the formation and refinement of brain circuits and their functions in adulthood. One of the greatest challenges of present neuroscience is to try to explain how synaptic connections change and cortical maps are formed and modified to generate the most suitable adaptive behavior after different external stimuli. Adenosine is emerging as a key player in these plastic changes at different brain areas. Here, we review the current knowledge of the mechanisms responsible for the induction and duration of synaptic plasticity at different postnatal brain development stages in which adenosine, probably released by astrocytes, directly participates in the induction of long-term synaptic plasticity and in the control of the duration of plasticity windows at different cortical synapses. In addition, we comment on the role of the different adenosine receptors in brain diseases and on the potential therapeutic effects of acting via adenosine receptors.

It is a widely held opinion that sleep is important for human brain health. Here we examine the evidence for this view, focusing on normal variations in sleep patterns. We discuss the functions of sleep and highlight the paradoxical implications of theories seeing sleep as an adaptive capacity versus the theory that sleep benefits clearance of metabolic waste from the brain. We also evaluate the proposition that sleep plays an active role in consolidation of memories. Finally, we review research on possible effects of chronic sleep deprivation on brain health. We find that the evidence for a causal role of sleep in human brain health is surprisingly weak relative to the amount of attention to sleep in science and society. While there are well-established associations between sleep parameters and aspects of brain health, results are generally not consistent across studies and measures, and it is not clear to what extent alterations in sleep patterns represent symptoms or causes. Especially, the proposition that long sleep (>8 hours) in general is beneficial for long-term brain health in humans seems to lack empirical support. We suggest directions for future research to establish a solid foundation of knowledge about a role of sleep in brain health based on longitudinal studies with frequent sampling, attention to individual differences, and more ecologically valid intervention studies.

The legacy of Santiago Ramón y Cajal, Spain's first Nobel laureate neuroscientist recognized as the founding father of modern neuroscience, is to be preserved in a new museum in Madrid: the National Museum of Natural Sciences (MNCN), one of the most important scientific research institutes in the country sciences in the scope of natural sciences of the Spanish National Research Council. For a boy who dreamed of being an artist but started his career apprenticed to first a barber and then a cobbler, Santiago Ramón y Cajal made a distinguished mark in science. One of Cajal's most important contributions to our understanding of the brain was his discovery of the direction of the information flow within neurons and in neural circuits, which he called the "dynamic polarization law," without a doubt the founding principle of neurosciences. The exposition planned by the MNCN is a perfect occasion to show the academy and, it is hoped, the general public at large the beautiful organization of the nervous system as first acknowledged by modern science. With the highly motivated organizers of this well-planned initiative, neuroscientists at the Cajal Institute are confident that this sample of the Cajal legacy will also be taken as an esthetic experience for those who approach it for the first time. It might be that science and art often go together.

Interneurons (INs) play a crucial role in the regulation of neural activity within the medial prefrontal cortex (mPFC), a brain region critically involved in executive functions and behavioral control. In recent preclinical studies, dysregulation of INs in the mPFC has been implicated in the pathophysiology of substance use disorder, characterized by vulnerability to chronic drug use. Here, we explore the diversity of mPFC INs and their connectivity and roles in vulnerability to addiction. We also discuss how these INs change over time with drug exposure. Finally, we focus on noninvasive brain stimulation as a therapeutic approach for targeting INs in substance use disorder, highlighting its potential to restore neural circuits.

Swelling, stiffness, and pain in synovial joints are primary hallmarks of osteoarthritis and rheumatoid arthritis. Hyperactivity of nociceptors and excessive release of inflammatory factors and pain mediators play a crucial role, with emerging data suggesting extensive remodelling and plasticity of joint innervations. Herein, we review structural, functional, and molecular alterations in sensory and autonomic axons wiring arthritic joints and revisit mechanisms implicated in the sensitization of nociceptors, leading to chronic pain. Sprouting and reorganization of sensory and autonomic fibers with the invasion of ectopic branches into surrounding inflamed tissues are associated with the upregulation of pain markers. These changes are frequently complemented by a phenotypic switch of sensory and autonomic profiles and activation of silent axons, inferring homeostatic adjustments and reprogramming of innervations. Identifying critical molecular players and neurobiological mechanisms underpinning the rewiring and sensitization of joints is likely to elucidate causatives of neuroinflammation and chronic pain, assisting in finding new therapeutic targets and opportunities for interventions.

The refinement of immature neuronal networks into efficient mature ones is critical to nervous system development and function. This process of synapse refinement is driven by the neuronal activity-dependent competition of converging synaptic inputs, resulting in the elimination of weak inputs and the stabilization of strong ones. Neuronal activity, whether in the form of spontaneous activity or experience-evoked activity, is known to drive synapse refinement in numerous brain regions. More recent studies are now revealing the manner and mechanisms by which neuronal activity is detected and converted into molecular signals that appropriately regulate the elimination of weaker synapses and stabilization of stronger ones. Here, we highlight how spontaneous activity and evoked activity instruct neuronal activity-dependent competition during synapse refinement. We then focus on how neuronal activity is transformed into the molecular cues that determine and execute synapse refinement. A comprehensive understanding of the mechanisms underlying synapse refinement can lead to novel therapeutic strategies in neuropsychiatric diseases characterized by aberrant synaptic function.

Swedish neuroscientist Bror Anders Rexed lived between 1914 and 2002. He was a renowned neuroscientist and a politician who packed a lot into his 88-year life. Bror Rexed is best known for his works on the description of the cytoarchitectonic organization of the cat spinal cord. Rexed laminae as an eponym is a historical landmark for the spinal cord cytoarchitecture. Rexed's name (particularly his surname) has also been linked to the du-reform in Swedish. In this article, we focus on his works on the central and peripheral nervous systems and translational approaches for neurosurgery, as well as his influence on health policies in Sweden.

The brain has the powerful ability to transform experiences into anatomic maps and continuously integrate massive amounts of information to form new memories. The manner in which the brain performs these processes has been investigated extensively for decades. Emerging reports suggest that dendritic spines are the structural basis of information storage. The complex orchestration of functional and structural dynamics of dendritic spines is associated with learning and memory. Owing to advancements in techniques, more precise observations and manipulation enable the investigation of dendritic spines and provide clues to the challenging question of how memories reside in dendritic spines. In this review, we summarize the remarkable progress made in revealing the role of dendritic spines in fear memory and the techniques used in this field.

The cerebellum and its thalamic projections to the primary motor cortex (M1) are well known to play an essential role in executing daily actions. Anatomic investigations in animals and postmortem humans have established the reciprocal connections between these regions; however, how these pathways can shape cortical activity in behavioral contexts and help promote recovery in neuropathological conditions remains not well understood. The present review aims to provide a comprehensive description of these pathways in animals and humans and discuss how novel noninvasive brain stimulation (NIBS) methods can be used to gain a deeper understanding of the cerebellar-M1 connections. In the first section, we focus on recent animal literature that details how information sent from the cerebellum and thalamus is integrated into an broad network of cortical motor neurons. We then discuss how NIBS approaches in humans can be used to reliably assess the connectivity between the cerebellum and M1. Moreover, we provide the latest perspectives on using advanced NIBS approaches to investigate and modulate multiple cerebellar-cortical networks involved in movement behavior and plasticity. Finally, we discuss how these emerging methods have been used in translation research to produce long-lasting modifications of cerebellar-thalamic-M1 to restore cortical activity and motor function in neurologic patients.

The cerebral cortex develops through a carefully conscripted series of cellular and molecular events that culminate in the production of highly specialized neuronal and glial cells. During development, cortical neurons and glia acquire a precise cellular arrangement and architecture to support higher-order cognitive functioning. Decades of study using rodent models, naturally gyrencephalic animal models, human pathology specimens, and, recently, human cerebral organoids, reveal that rodents recapitulate some but not all the cellular and molecular features of human cortices. Whereas rodent cortices are smooth-surfaced or lissencephalic, larger mammals, including humans and nonhuman primates, have highly folded/gyrencephalic cortices that accommodate an expansion in neuronal mass and increase in surface area. Several genes have evolved to drive cortical gyrification, arising from gene duplications or de novo origins, or by alterations to the structure/function of ancestral genes or their gene regulatory regions. Primary cortical folds arise in stereotypical locations, prefigured by a molecular "blueprint" that is set up by several signaling pathways (e.g., Notch, Fgf, Wnt, PI3K, Shh) and influenced by the extracellular matrix. Mutations that affect neural progenitor cell proliferation and/or neurogenesis, predominantly of upper-layer neurons, perturb cortical gyrification. Below we review the molecular drivers of cortical folding and their roles in disease.