Neuroscience
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Microglia play an ambiguous role in injury or repair after ischemia-reperfusion, and the induced oxidative stress serves as an important signal, mediates direct toxicity to nerve cells, and eventually simulates complex physiological processes such as activation of microglia to repair the damaged area. Herein, we show that sprouty-related protein with an EVH1 domain 1 (SPRED1) may act as a regulatory node in this phenomenon. The ischemic brain of an ischemia-reperfusion rat model constructed by middle cerebral artery occlusion (MCAO) showed an increase in oxidative stress and downregulation of SPRED1 expression. ⋯ In the absence of H2O2 induction, SPRED overexpression alone did not mediate such an effect. These findings indicate that SPRED1 tends to maintain intracellular homeostasis of signals, but the oxidative stress derived from ischemia-reperfusion can easily degrade SPRED1 and consequently re-activate these restricted signals and alter the behavior of microglia. Thus, our study reveals a novel role of SPRED1 in microglia in response to cerebral ischemia-induced oxidative stress.
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Bipolar disorder may begin as depression or mania, which can affect the treatment and prognosis of bipolar disorder. However, the physiological and pathological differences of pediatric bipolar disorder (PBD) patients with different onset symptoms are not clear. The purpose of this study was to investigate the differences of clinical, cognitive function and intrinsic brain networks in PBD patients with first-episode depression and first-episode mania. ⋯ And significant associations of brain activity with clinical assessments or cognition were found in different patients. In conclusion, we found differential impairments in cognitive and brain network activation in first-episode depressive and first-episode manic PBD patients, and correlations were found between these impairments. These evidences may shed light on the different developmental paths of bipolar disorder.
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Cell quiescence is an essential mechanism that allows cells to temporarily halt proliferation while preserving the potential to resume it at a later time. The molecular mechanisms underlying cell quiescence are complex and involve the regulation of various signaling pathways, transcription factors and epigenetic modifications. The importance of unveiling the mechanisms regulating the quiescent state is undeniable, as its long-term maintenance is key to sustain tissue homeostasis throughout life. ⋯ Differently from other non-proliferative states, quiescence is a reversible and tightly regulated condition that can re-activate to support the formation of new neurons throughout adult lifespan. Decoding its regulatory mechanisms in homeostasis and unveiling how it is modulated in the context of the aged brain or during tumorigenesis, could bring us closer to the development of new potential strategies to intervene in adult neurogenesis with therapeutic purposes. Starting with a general conceptualization of the quiescent state in different stem cell niches, we here review what we have learned about NSC quiescence in the SEZ, encompassing the experimental strategies used for its study, to end up discussing the modulation of quiescence in the context of a physiology or pathological NSC dysregulation.
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Sensory systems in the peripheral and central nervous systems shape host response during infections.
The function of sensory cells has been largely investigated in the field of neuroscience for how they report the physical and chemical changes of the environment ("exteroception") and of internal physiology ("interoception"). Investigations over the last century have largely focused on the morphological, electrical and receptor properties of sensory cells in the nervous system focusing on conscious perception of external cues or homeostatic regulation upon detection of internal cues. ⋯ The corresponding neuronal activation associated with the presence of pathogens can impact their classical functions within the nervous system and trigger the release of compounds modulating the response to intruders, either triggering pain to raise awareness, enhancing host defense or sometimes, aggravating the infection. This perspective brings to light the need for interdisciplinary training in immunology, microbiology and neuroscience for the next generation of investigators in this field.
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Dopamine (DA) is a critical neuromodulator involved in various brain functions. To understand how DA regulates neural circuits and behaviors in the physiological and pathological conditions, it is essential to have tools that enable the direct detection of DA dynamics in vivo. Recently, genetically encoded DA sensors based on G protein-coupled receptors revolutionized this field, as it allows us to track in vivo DA dynamic with unprecedented spatial-temporal resolution, high molecular specificity, and sub-second kinetics. ⋯ Then we focus on the development of genetically encoded DA sensors and feature its significance to understanding dopaminergic neuromodulation across diverse behaviors and species. Finally, we present our perspectives about the future direction of the next-generation DA sensors and extend their potential applications. Overall, this review offers a comprehensive perspective on the past, present, and future of DA detection tools, with important implications for the study of DA functions in health and disease.