Neuroscience
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Animals use multiple strategies to maintain spatial orientation. Dead reckoning is a form of spatial navigation that depends on self-movement cue processing. During dead reckoning, the generation of self-movement cues from a starting position to an animal's current position allow for the estimation of direction and distance to the position movement originated. ⋯ Disruptions in exploratory behavior associated with medial frontal lesions were consistent with impaired motor coordination, response inhibition, or egocentric reference frame. These processes are necessary for spatial orientation; however, they are not sufficient for self-movement cue processing. Therefore it is possible that the medial frontal cortex provides processing resources that support dead reckoning in other brain structures but does not of itself compute the kinematic details of dead reckoning.
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Adult neurogenesis participates in fish olfaction sensitivity in response to environmental challenges. Therefore, we investigated if several populations of stem/progenitor cells that are retained in the olfactory bulbs (OB) may constitute different neurogenic niches that support growth and functional demands. By electron microscopy and combination cell proliferation and lineage markers, we found that the telencephalic ventricle wall (VW) at OB level of Austrolebias charrua fish presents three neurogenic niches (transitional 1, medial 2 and ventral 3). ⋯ Scanning electron microscopy evidenced that the whole VW has only monociliated cells with remarkable differences in cilium length among regions. In OB there are monociliated cells with dwarf cilium whereas ventral telencephalon shows long cilium. Summarizing, we identified three neurogenic niches that might serve different functional purposes.
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Currently available evidence indicates that neurons containing melanin-concentrating hormone (MCH) in the lateral hypothalamus are critical modulators of sleep-wakefulness, but their precise role in this function is not clear. Studies employing optogenetic stimulation of MCH neurons have yielded inconsistent results, presumably due to differences in the optogenetic stimulation protocols, which do not approximate normal patterns of cell firing. ⋯ On the other hand, selective deletions of MCH neurons altered the diurnal rhythm of wake and REM sleep without altering their total amounts. These results indicate that activation of MCH neurons primarily drives REM sleep and their presence may be necessary for normal expression of diurnal variation of REM sleep and wake.
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Resting state functional magnetic resonance imaging (rsfMRI) has been extensively applied to investigate the organization of functional networks in the brain. As an essential part of the central nervous system (CNS), the spinal cord has not been well explored about its intrinsic functional network. In this study, we aim to thoroughly investigate the characteristics of the intrinsic functional network in the spinal cord using rsfMRI. ⋯ The present results revealed the significance of the upper cervical cord in the intrinsic functional network of the human cervical spinal cord. In addition, this study demonstrated the efficiency of the cervical spinal cord functional network and the reproducibility of rsfMRI analysis on the spinal cord was also confirmed. As knowledge expansion of intrinsic functional network from the brain to the spinal cord, this study shed light on the organization of the spinal cord functional network in both normal development and clinical disorders.
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Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by beta-amyloid (Aβ) deposition, neurofibrillary tangles and cognitive decline. Recent pharmacologic studies have found that ATP-sensitive potassium (KATP) channels may play a role in AD and could be a potential therapeutic target. Interestingly, these channels are found in both neurons and astrocytes. ⋯ Dual immunofluorescence revealed a dramatic increase in co-localization of Kir6.2-IR and GFAP-IR. Taken together, these data demonstrate that increased Kir6.2 is seen in reactive astrocytes in old 3xTg-AD mice and human AD tissue. These changes could dramatically alter astrocytic function and subsequently contribute to AD phenotype in either a compensatory or pathophysiological manner.