Neuroscience
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Zebrafish (Danio rerio) is currently in vogue as a prevalently used experimental model for studies concerning neurobehavioural disorders and associated fields. Since the 1960s, this model has succeeded in breaking most barriers faced in the hunt for an experimental model. From its appearance to its high parity with human beings genetically, this model renders itself as an advantageous experimental lab animal. ⋯ The tools, techniques, protocols, and apparatuses that bolster zebrafish studies are discussed. The probable research that can be done using zebrafish has also been briefly outlined. The various breeding and maintenance methods employed, along with the information on various strains available and most commonly used, are also elaborated upon, supplementing Zebrafish's use in neuroscience.
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Tibetans have adapted to high altitude environments. However, the genetic effects in their brains have not been identified. Twenty-five native Tibetans living in Lhasa (3650 m) were recruited for comparison with 20 Han immigrants who originated from lowlands and had been living in Lhasa for two years. ⋯ Moreover, Tibetans have decreased functional connectivity (FC) between the left precentral gyrus and the frontal gyrusand right precuneus. In Tibetans and Han immigrants, hemoglobin and hematocrit were negatively correlated with total gray matter volume in males, SpO2 was also positively correlated with ALFF in the left fusiform gyrus, while hemoglobin, and hematocrit were positively correlated with VMHC in the precentral gyrus and FC in the precentral gyrus with other brain regions, SpO2 was also found to be negatively correlated with VMHC in the precentral gyrus, and hemoglobin and hematocrit were negatively correlated with ALFF in the left putamen and left fusiform gyrus. In summary, genetic mutations may result in modulation of some brain regions, which was further confirmed by the identification of correlations with hemoglobin and hematocrit in these regions.
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Fatigue is a long-lasting problem in traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD), with limited research that investigated the fatigue-related white-matter changes within TBI and/or PTSD cohorts. This exploratory cross-sectional study used diffusion tensor imaging (DTI) and neuropsychological data collected from 153 male Vietnam War veterans, as part of the Alzheimer's Disease Neuroimaging Initiative - Department of Defense, and were divided clinically into control veterans, PTSD, TBI, and with both TBI and PTSD (TBI + PTSD). The existence of fatigue was defined by the question "Do you often feel tired, fatigued, or sleepy during the daytime?". ⋯ Compared to non-fatigued subgroups, no white-matter differences were observed in the fatigued subgroups of control or TBI, while the fatigued PTSD subgroup only showed increased diffusivity measures (i.e., radial and axial), and the fatigued TBI + PTSD subgroup showed decreased fractional anisotropy and increased diffusivity measures (PFWE ≤ 0.05). The results act as preliminary findings suggesting fatigue to be significantly reported in TBI + PTSD and PTSD decades post-trauma with a possible link to white-matter microstructural differences in both PTSD and TBI + PTSD. Future studies with larger cohorts and detailed fatigue assessments would be required to identify the white-matter changes associated with fatigue in these cohorts.
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Dietary modifications often have a profound impact on the penetrance and expressivity of neurological phenotypes that are caused by genetic defects. Our previous studies in Drosophila melanogaster revealed that seizure-like phenotypes of gain-of-function voltage-gated sodium (Nav) channel mutants (paraShu, parabss1, and paraGEFS+), as well as other seizure-prone "bang-sensitive" mutants (eas and sda), were drastically suppressed by supplementation of a standard diet with milk whey. In the current study we sought to determine which components of milk whey are responsible for the diet-dependent suppression of their hyperexcitable phenotypes. ⋯ Given that lipid supplementation during the larval stages effectively suppressed adult paraShu phenotypes, dietary lipids likely modify neural development to compensate for the defects caused by the mutations. Consistent with this notion, lipid feeding fully rescued abnormal dendrite development of class IV sensory neurons in paraShu larvae. Overall, our findings demonstrate that milk lipids are sufficient to ameliorate hyperexcitable phenotypes in Drosophila mutants, providing a foundation for future investigation of the molecular and cellular mechanisms by which dietary lipids modify genetically induced abnormalities in neural development, physiology, and behavior.