Trends in Neurosciences最新文献

Neurodegenerative disorders represent a leading cause of disability among the elderly population, and Parkinson's disease (PD) is the second most prevalent. Emerging evidence suggests a frequent co-occurrence of circadian disruption and PD. However, the nature of this relationship remains unclear: is circadian disruption a cause, consequence, or a parallel feature of the disease that shares the same root cause? This review seeks to address this question by highlighting and discussing clinical evidence and findings from experiments using vertebrate and invertebrate animal models. While research on causality is still in its early stages, the available data suggest reciprocal interactions between PD progression and circadian disruption.

Recent studies in non-human primates do not find pronounced signals related to the animal's own body movements in the responses of neurons in the visual cortex. This is notable because such pronounced signals have been widely observed in the visual cortex of mice. Here, we discuss factors that may contribute to the differences observed between species, such as state, slow neural drift, eccentricity, and changes in retinal input. The interpretation of movement-related signals in the visual cortex also exemplifies the challenge of identifying the sources of correlated variables. Dissecting these sources is central for understanding the functional roles of movement-related signals. We suggest a functional classification of the possible sources, aimed at facilitating cross-species comparative approaches to studying the neural mechanisms of vision during natural behavior.

In pancreatic cancer, significant alterations occur in the local nervous system, including axonogenesis, neural remodeling, perineural invasion, and perineural neuritis. Pancreatic cancer can impact the central nervous system (CNS) through cancer cell-intrinsic factors or systemic factors, particularly in the context of cancer cachexia. These peripheral and central neuropathic changes exert substantial influence on cancer initiation and progression. Moreover, chemotherapy-induced neuropathy is common in pancreatic cancer, causing peripheral nerve damage and cognitive dysfunction. Targeting the crosstalk between pancreatic cancer and the nervous system, either peripherally or centrally, holds promise in cancer treatment, pain relief, and improved quality of life. Here, we summarize recent findings on the molecular mechanisms behind these neuropathic changes in pancreatic cancer and discuss potential intervention strategies.

In a recent study, Haas, Bravo, and colleagues integrated optogenetic stimulation with simultaneous functional in vivo positron emission tomography (PET)/magnetic resonance imaging (MRI) measurements in rats. By activating the nigrostriatal pathway in the substantia nigra pars compacta (SNc), they observed concurrent metabolic and hemodynamic fluctuations associated with the dopaminergic pathway in living animals at the whole-brain level.

Across species, social behaviors are shaped and maintained through positive reinforcement of affiliative social interactions. As with nonsocial rewards, the reinforcing properties of social interactions have been shown to involve interplay between various brain regions and the mesolimbic reward system. In this review, we summarize findings from rodent research on the neural circuits that encode and mediate different components of social reward-seeking behavior. We explore methods to parse and study social reward-related behaviors using available behavioral paradigms. We also compare the neural mechanisms that support social versus nonsocial reward-seeking. Finally, we discuss how internal state and neuromodulatory systems affect reward-seeking behavior and the neural circuits that underlie social reward.

The orbitofrontal cortex (OFC) and ventromedial-prefrontal cortex (vmPFC) play a key role in decision-making and encode task states in addition to expected value. We review evidence suggesting a connection between value and state representations and argue that OFC / vmPFC integrate stimulus, context, and outcome information. Comparable encoding principles emerge in late layers of deep reinforcement learning (RL) models, where single nodes exhibit similar forms of mixed-selectivity, which enables flexible readout of relevant variables by downstream neurons. Based on these lines of evidence, we suggest that outcome-maximization leads to complex representational spaces that are insufficiently characterized by linear value signals that have been the focus of most prior research on the topic. Major outstanding questions concern the role of OFC/ vmPFC in learning across tasks, in encoding of task-irrelevant aspects, and the role of hippocampus-PFC interactions.

Cortical activity is constantly fluctuating between distinct spatiotemporal activity patterns denoted by changes in brain state. States of cortical desynchronization arise during motor generation, increased attention, and high cognitive load. Synchronized brain states comprise spatially widespread, coordinated low-frequency neural activity during rest and sleep when disengaged from the external environment or 'offline'. The claustrum is a small subcortical structure with dense reciprocal connections with the cortex suggesting modulation by, or participation in, brain state regulation. Here, we highlight recent work suggesting that neural activity in the claustrum supports cognitive processes associated with synchronized brain states characterized by increased low-frequency network activity. As an example, we outline how claustrum activity could support episodic memory consolidation during sleep.

Cellular senescence is a cell state characterized by resistance to apoptosis and stable cell cycle arrest. Senescence was first observed in mitotic cells in vitro. Recent evidence from in vivo studies and human tissue indicates that postmitotic cells, including neurons, may also become senescent. The quiescent cell state of neurons and inconsistent descriptions of neuronal senescence across studies, however, have caused confusion in this burgeoning field. We summarize evidence demonstrating that exit from G₀ quiescence may protect neurons against apoptosis and predispose them toward senescence. Additionally, we propose the term 'neurescent' for senescent neurons and introduce the cell state, G_X, to describe cell cycle arrest achieved by passing through G₀ quiescence. Criteria are provided to identify neurescent cells, distinguish them from G₀ quiescent neurons, and compare neurescent phenotypes with classic replicative senescence.

Although zebrafish (Danio rerio) neuroscience research is rapidly expanding, the fundamental question of how these fish should be maintained in research laboratories remains largely unstudied. This may explain the diverse practices and broad range of environmental parameters used in zebrafish facilities. Here, we provide examples of these parameters and practices, including housing density, tank size, and water chemistry. We discuss the principles of stochastic resonance versus homeostasis and provide hypothetical examples to explain why keeping zebrafish outside of their tolerated range of environmental parameters may increase phenotypical variance and reduce replicability. We call for systematic studies to establish the optimal maintenance conditions for zebrafish. Furthermore, we discuss why knowing more about the natural behavior and ecology of this species could be a guiding principle for these studies.

Recent work by Wu and colleagues unveiled a previously enigmatic population of spleen-innervating nociceptors from left T8-T13 dorsal root ganglia (DRGs) in mice. They found a specific DRG-spleen sensorineural connection that promotes humoral immunity via a CGRP-CALCRL/RAMP1 axis, providing a valuable target for immune regulation in local microenvironments.