Trends in Neurosciences最新文献

Migraine is highly prevalent and debilitating. The persistent headaches in this condition are thought to arise from the activation and sensitization of the trigeminovascular pathway. Both clinical and animal model studies have suggested that neuroimmune interactions contribute to the pathophysiology of migraine headache. In this review, we first summarize the findings from human studies implicating the dysregulation of the immune system in migraine, including genetic analyses, measurement of circulatory factors, and neuroimaging data. We next discuss recent advances from rodent studies aimed at elucidating the neuroimmune interactions that manifest at various levels of the trigeminovascular pathway and lead to the recruitment of innate and adaptive immune cells as well as immunocompetent glial cells. These cells reciprocally modulate neuronal activity via multiple pro- and anti-inflammatory mediators, thereby regulating peripheral and central sensitization. Throughout the discussions, we highlight the potential clinical and translational implications of the findings.

Stress-related disorders are among the biggest global health challenges. Despite significant progress in understanding their neurocognitive basis, the promise of applying insights from fundamental research to prevention and treatment remains largely unfulfilled. We argue that neurofeedback – a method for training voluntary control over brain activity – has the potential to fill this translational gap. We provide a contemporary perspective on neurofeedback as endogenous neuromodulation that can target complex brain network dynamics, is transferable to real-world scenarios outside a laboratory or treatment facility, can be trained prospectively, and is individually adaptable. This makes neurofeedback a prime candidate for a personalized preventive neuroscience-based intervention strategy that focuses on the ecological momentary neuromodulation of stress-related brain networks in response to actual stressors in real life.

Many animal species use olfaction to extract information about objects in their environment. Yet, the specific molecular signature that any given object emits varies due to various factors. Here, we detail why such variability makes chemosensory-mediated object recognition such a hard problem, and we propose that a major function of the elaborate chemosensory network is to overcome it. We describe previous work addressing different elements of the problem and outline future research directions that we consider essential for a full understanding of object-oriented olfaction. In particular, we call for extensive representation of olfactory object variability in chemical, behavioral, and electrophysiological analyses. While written with an emphasis on macrosmatic mammalian species, our arguments apply to all organisms that employ chemosensation to navigate complex environments.

A major aim of neuroscience is to identify and model the functional properties of neural cells whose dysfunction underlie neuropsychiatric illness. In this article, we propose that human-derived monoclonal autoantibodies (HD-mAbs) are well positioned to selectively target and manipulate neural subpopulations as defined by their protein expression; that is, cellular proteotypes. Recent technical advances allow for efficient cloning of autoantibodies from neuropsychiatric patients. These HD-mAbs can be introduced into animal models to gain biological and pathobiological insights about neural proteotypes of interest. Protein engineering can be used to modify, enhance, silence, or confer new functional properties to native HD-mAbs, thereby enhancing their versatility. Finally, we discuss the challenges and limitations confronting HD-mAbs as experimental research tools for neuroscience.

Neuroinflammation is a feature of both neurodegenerative disease and normal brain aging. The roles of type I interferon (IFN-I) in the aged brain are incompletely understood. A recent article by Roy et al. reveals pervasive IFN-I activity in normal mouse brain aging, and highlights the importance of microglial IFN-I signaling in neuroinflammation.

A recent study by Wu, Podvalny, and colleagues investigated how ongoing spontaneous brain activity interacts with sensory input and shapes conscious perception. It reports diverse effects of prestimulus activity in several key networks, revealing new roles of the prefrontal cortex and the default mode network in perception and consciousness.

The human voice is a potent social signal and a distinctive marker of individual identity. As individuals go through puberty, their voices undergo acoustic changes, setting them apart from others. In this article, we propose that hormonal fluctuations in conjunction with morphological vocal tract changes during puberty establish a sensitive developmental phase that affects the monitoring of the adolescent voice and, specifically, self-other distinction. Furthermore, the protracted maturation of brain regions responsible for voice processing, coupled with the dynamically evolving social environment of adolescents, likely disrupts a clear differentiation of the self-voice from others' voices. This socioneuroendocrine framework offers a holistic understanding of voice monitoring during adolescence.

Recent work by Giusti and colleagues showed that circTulp4 modulates excitatory synaptic strength. Knocking down circTulp4 disrupts the excitation-inhibition (E/I) balance in mice and leads to hypersensitivity toward aversive stimuli. These observations update our appreciation of the functions of circular (circ)RNA in the nervous system and their potential implication in neurodevelopmental and neuropsychiatric disorders.