Neuroscientist最新文献

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 beginnings of cybernetics were marked by the publication of two papers in 1943. In the first one, Rosenblueth, Wiener, and Bigelow claimed that purposeful behavior is a circular process controlled by negative feedback. In the second seminal paper, McCulloch and Pitts proposed that neurons are interconnected working as logical operators. Both articles raised human-machine analogies and mathematically formulated cognitive mechanisms. These ideas ignited the interest of von Neumann, who was developing the first stored-program computer. Thus, after a preliminary meeting in 1945, a series of meetings were held between 1946 and 1953. The role of the Spanish neurophysiologist Rafael Lorente de Nó in the beginnings of cybernetics is attested not only by his participation in the core members of these Macy conferences but also for his previous description of reverberating circuits formed by a closed chain of internuncial neurons. This was the first neurobiologic demonstration of a feedback loop. Most researchers considered the central nervous system as a mere reflex organ until then; nevertheless, he demonstrated a self-sustained central activity in the nervous system, supporting the idea of self-regulating mechanisms as a key concept not just in machines but also in the brain.

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.

Pioneering investigations in the mid-19th century revealed that the perception of tactile cues presented to the surface of the skin improves with training, which is referred to as tactile learning. Surprisingly, tactile learning also occurs for body parts and skin locations that are not physically involved in the training. For example, after training of a finger, tactile learning transfers to adjacent untrained fingers. This suggests that the transfer of tactile learning follows a somatotopic pattern and involves brain regions such as the primary somatosensory cortex (S1), in which the trained and untrained body parts and skin locations are represented close to each other. However, other results showed that transfer occurs between body parts that are not represented close to each other in S1-for example, between the hand and the foot. These and similar findings have led to the suggestion of additional cortical mechanisms to explain the transfer of tactile learning. Here, different mechanisms are reviewed, and the extent to which they can explain the transfer of tactile learning is discussed. What all of these mechanisms have in common is that they assume a representational or functional relationship between the trained and untrained body parts and skin locations. However, none of these mechanisms alone can explain the complex pattern of transfer results, and it is likely that different mechanisms interact to enable transfer, perhaps in concert with higher somatosensory and decision-making areas.

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.