Neuroscientist最新文献

Harnessing intelligence from brain cells in vitro requires a multidisciplinary approach integrating wetware, hardware, and software. Wetware comprises the in vitro brain cells themselves, where differentiation from induced pluripotent stem cells offers ethical scalability; hardware typically involves a life support system and a setup to record the activity from and deliver stimulation to the brain cells; and software is required to control the hardware and process the signals coming from and going to the brain cells. This review provides a broad summary of the foundational technologies underpinning these components, along with outlining the importance of technology integration. Of particular importance is that this new technology offers the ability to extend beyond traditional methods that assess primarily the survival and spontaneous activity of neural cultures. Instead, the focus returns to the core function of neural tissue: the neurocomputational ability to process information and respond accordingly. Therefore, this review also covers work that, despite the relatively early state of current technology, has provided novel and meaningful understandings in the field of neuroscience along with opening exciting avenues for future research.

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.

Recent electron microscopy reveals that weak synaptic connectivity predominates in the human cerebral cortex, raising the question of how information is transmitted by action potentials in these neural networks. Differences in field potential oscillations (brainwaves) and glia between vertebrates and invertebrates provide a possible answer that can also account for the incomparable increase in the cognitive ability of vertebrates.

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.

Microglia serve as vital innate immune cells in the central nervous system, playing crucial roles in the generation and development of brain neurons, as well as mediating a series of immune and inflammatory responses. The morphologic transitions of microglia are closely linked to their function. With the advent of single-cell sequencing technology, the diversity of microglial subtypes is increasingly recognized. The intricate interactions between microglia and neuronal networks have significant implications for psychiatric disorders and neurodegenerative diseases. A deeper investigation of microglia in neurologic diseases such as Alzheimer disease, depression, and epilepsy can provide valuable insights in understanding the pathogenesis of diseases and exploring novel therapeutic strategies, thereby addressing issues related to central nervous system disorders.

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.

As a monovalent cation channel, the transient receptor potential melastatin 4 (TRPM4) channel is a unique member of the transient receptor potential family. Abnormal TRPM4 activity has been identified in various neurologic disorders, such as stroke, spinal cord injury, traumatic brain injury, multiple sclerosis, amyotrophic lateral sclerosis, pathologic pain, and epilepsy. Following brain hypoxia/ischemia and inflammation, TRPM4 up-regulation and enhanced activity contribute to the cell death of neurons, vascular endothelial cells, and astrocytes. Enhanced ionic influx via TRPM4 leads to cell volume increase and oncosis. Depolarization of membrane potential following TRPM4 activation and interaction between TRPM4 and N-methyl-d-aspartate receptors exacerbate excitotoxicity during hypoxia. Importantly, TRPM4 expression and activity remain low in healthy neurons, making it an ideal drug target. Current approaches to inhibit or modulate the TRPM4 channel have various limitations that hamper the interpretation of TRPM4 physiology in the nervous system and potentially hinder their translation into therapy. In this review, we discuss the pathophysiologic roles of TRPM4 and the different inhibitors that modulate TRPM4 activity for potential treatment of neurologic diseases.