Neuroscience
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It is commonly recognized that physical exercise positively affects several CNS regions and improves cognitive abilities. For example, exercise is associated with an increase in neurogenesis and facilitation of long-term potentiation in the hippocampus. Conversely, animal models for depression are associated with a decrease in neurogenesis and a reduction of long-term potentiation in the hippocampus. ⋯ Unexpectedly, in dexamethasone-exposed animals, dentate gyrus long-term potentiation was facilitated, whereas long-term potentiation in CA1 was unaffected by prenatal dexamethasone or by 10 or 21 days of voluntary running. Irrespective of age, prenatal dexamethasone and running had limited effects on synaptic transmission and presynaptic release in CA1 and dentate gyrus. In summary, running facilitates dentate gyrus long-term potentiation in adult animals that resembles the effects of prenatal dexamethasone.
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Defective cortical processing of visual stimuli and altered retinal function have been described in autism spectrum disorder (ASD) patients. In keeping with these findings, anatomical and functional defects have been found in the visual cortex and retina of mice bearing mutations for ASD-associated genes. Here we sought to investigate the anatomy and function of the adult retina of Engrailed 2 knockout (En2-/-) mice, a model for ASD. ⋯ In addition, En2-/- adult mice showed a significant reduction of photoreceptor (rhodopsin) and bipolar cell (Pcp2, PKCα) markers. Functional defects were also present in the retina of En2 mutants, as indicated by electroretinogram recordings showing a significant reduction in both a-wave and b-wave amplitude in En2-/- mice as compared to controls. These data show for the first time that anatomical and functional defects are present in the retina of the En2 ASD mouse model.
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Lipoxin A4 (LXA4) has been reported to reduce inflammation in experimental subarachnoid hemorrhage (SAH), but the mechanism remains unclear. In this study, we investigated the role of LXA4 in inflammation-mediated cerebrovascular endothelial dysfunction and the potential mechanism after SAH. SAH was induced by endovascular perforation in male Sprague-Dawley rats, and recombinant LXA4 was injected intracerebroventricularly 1.5 h after the operation. ⋯ The administration of LXA4 significantly ameliorated endothelial dysfunction, recovered microflow, and suppressed the inflammation and infiltration of neutrophils in SAH rats. The underlying mechanism of this outcome may involve the LXA4/FPR2/ERK1/2 pathway. LXA4 might be a promising candidate for acute SAH treatment.
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In the auditory system, distinct and reproducible transient activities responding to the onset of sound have long been the focus when characterizing the auditory cortex, i.e., tonotopic maps, subregions, and layer-specific representation. There is limited information on sustained activities because the rapid adaptation impairs reproducibility and the signal-to-noise ratio. We recently overcame this problem by focusing on neural synchrony and machine learning demonstrated that band-specific power and the phase locking value (PLV) represent sound information in a tonotopic and region-specific manner. ⋯ SLR achieved the highest discrimination performance in high-gamma activities in layers 4 and 5/6, higher than in layer 2/3, indicating poor sound representation in layer 2/3. Moreover, the recording sites that contributed to the discrimination in layers 4 and 5/6 had a characteristic frequency similar to the test frequency and were often located in the belt area, indicating tonotopic and region-specific representation. These results indicate that information processing of sustained activities may depend on high-gamma oscillators, i.e., cortical inhibitory interneurons, and reflects layer-specific thalamocortical and corticocortical neural circuits in the auditory system, which may contribute to associative information processing beyond sound frequency in auditory perception.
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Environmental enrichment (EE) has been consistently reported to enhance cognitive function in mouse models of neuropathology. Microglia, implicated in Alzheimer's disease pathology, may mediate this effect. The aim of the present study was to investigate the effect of EE on cognitive function and microglia in mouse models of aging and amyloidosis. ⋯ APP/PS1 mice from EE had significantly (p = 0.01) higher colocalization of Iba1 and CD-68 labeling, indicative of increased phagocytic microglia compared to mice from SH. The findings of the present study suggest that EE after substantial brain amyloidosis, has the potential to preserve domains of cognitive function, while having no effect on Aβ deposition. The current study demonstrates that EE may attenuate microglia in aging APP/PS1 mice, and may promote alterations in cellular phenotype.