Neuroscientist最新文献

Extracellular vesicles (EVs) are secreted from most, if not all, cell types and are implicated in short- and long-distance signaling throughout the body. EVs are also secreted from neurons and represent an emergent neuronal communication platform. Understanding the functional implications of EV signaling to recipient neurons and glia requires understanding the cell biology involved in EV biogenesis, cargo loading, secretion, uptake, and signal transduction in the recipient cell. Here we review these major questions of EV biology while highlighting recent new insights and examples within the nervous system, such as modulating synaptic function or morphogenesis in recipient neurons.

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.

In the history of neuroscience, Cajal stands tall. Many figures in the late 19th and early 20th centuries made major contributions to neuroscience-Sherrington, Ferrier, Jackson, Holmes, Adrian, and Békésy, to name a few. But in the public mind, Cajal is unique. His application of the Golgi method, with an array of histologic stains, unlocked a wealth of new knowledge on the structure and function of the brain. Here we argue that Cajal's success should not only be attributed to the importance of his scientific contributions but also to the artistic visual language that he created and to his pioneering self-branding, which exploited methods of the artist, including classical drawing and the new invention of photography. We argue that Cajal created his distinctive visual language and self-branding strategy by interweaving an ostensibly objective research product with an intimately subjective narrative about the brain and himself. His approach is evident in the use of photography, notably self-portraits, which furthered broad engagement initially inspired by his scientific drawings. Through his visual language, Cajal made an impact in art and culture far beyond the bounds of science, which has sustained his scientific legacy.

The idea that the nervous system maintains a set point of network activity and homeostatically returns to that set point in the face of dramatic disruption-during development, after injury, in pathologic states, and during sleep/wake cycles-is rapidly becoming accepted as a key plasticity behavior, placing it alongside long-term potentiation and depression. The dramatic growth in studies of homeostatic synaptic plasticity of miniature excitatory synaptic currents (mEPSCs) is attributable, in part, to the simple yet elegant mechanism of uniform multiplicative scaling proposed by Turrigiano and colleagues: that neurons sense their own activity and globally multiply the strength of every synapse by a single factor to return activity to the set point without altering established differences in synaptic weights. We have recently shown that for mEPSCs recorded from control and activity-blocked cultures of mouse cortical neurons, the synaptic scaling factor is not uniform but is close to 1 for the smallest mEPSC amplitudes and progressively increases as mEPSC amplitudes increase, which we term divergent scaling. Using insights gained from simulating uniform multiplicative scaling, we review evidence from published studies and conclude that divergent synaptic scaling is the norm rather than the exception. This conclusion has implications for hypotheses about the molecular mechanisms underlying synaptic scaling.

Schizophrenia is a brain disorder that profoundly perturbs cognitive processing. Despite the success in treating many of its symptoms, the field lacks effective methods to measure and address its impact on reasoning, inference, and decision making. Prefrontal cortical abnormalities have been well documented in schizophrenia, but additional dysfunction in the interactions between the prefrontal cortex and thalamus have recently been described. This dysfunction may be interpreted in light of parallel advances in neural circuit research based on nonhuman animals, which show critical thalamic roles in maintaining and switching prefrontal activity patterns in various cognitive tasks. Here, we review this basic literature and connect it to emerging innovations in clinical research. We highlight the value of focusing on associative thalamic structures not only to better understand the very nature of cognitive processing but also to leverage these circuits for diagnostic and therapeutic development in schizophrenia. We suggest that the time is right for building close bridges between basic thalamic research and its clinical translation, particularly in the domain of cognition and schizophrenia.

Epilepsy is a common neurological disorder associated with alterations in cortical and subcortical brain networks. Despite a historical focus on gray matter regions involved in seizure generation and propagation, the role of white matter (WM) network disruption in epilepsy and its comorbidities has sparked recent attention. In this review, we describe patterns of WM alterations observed in focal and generalized epilepsy syndromes and highlight studies linking WM disruption to cognitive and psychiatric comorbidities, drug resistance, and poor surgical outcomes. Both tract-based and connectome-based approaches implicate the importance of extratemporal and temporo-limbic WM disconnection across a range of comorbidities, and an evolving literature reveals the utility of WM patterns for predicting outcomes following epilepsy surgery. We encourage new research employing advanced analytic techniques (e.g., machine learning) that will further shape our understanding of epilepsy as a network disorder and guide individualized treatment decisions. We also address the need for research that examines how neuromodulation and other treatments (e.g., laser ablation) affect WM networks, as well as research that leverages larger and more diverse samples, longitudinal designs, and improved magnetic resonance imaging acquisitions. These steps will be critical to ensuring generalizability of current research and determining the extent to which neuroplasticity within WM networks can influence patient outcomes.

Neural activities in local circuits exhibit complex and multilevel dynamic features. Individual neurons spike irregularly, which is believed to originate from receiving balanced amounts of excitatory and inhibitory inputs, known as the excitation-inhibition balance. The spatial-temporal cascades of clustered neuronal spikes occur in variable sizes and durations, manifested as neural avalanches with scale-free features. These may be explained by the neural criticality hypothesis, which posits that neural systems operate around the transition between distinct dynamic states. Here, we summarize the experimental evidence for and the underlying theory of excitation-inhibition balance and neural criticality. Furthermore, we review recent studies of excitatory-inhibitory networks with synaptic kinetics as a simple solution to reconcile these two apparently distinct theories in a single circuit model. This provides a more unified understanding of multilevel neural activities in local circuits, from spontaneous to stimulus-response dynamics.

The object of this article is a drawing by Peter Paul Rubens, a copy of "The Battle of Anghiari" by Leonardo da Vinci in 1503-1506. This work, created in 1603, was based on an engraving of 1553 by Lorenzo Zacchia, which was taken from a cartoon by Leonardo da Vinci. The original fresco itself is lost. The analysis of the drawing shows that the Peter Paul Rubens's copy of "The Battle of Anghiari" by Leonardo da Vinci, which was created six centuries ago, includes double content. The drawing depicting the battle secretly describes the three-dimensional image of the brain.