Neuroscience
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Multiple species display robust behavioral variance among individuals due to different genetic, genomic, epigenetic, neuroplasticity and environmental factors. Behavioral individuality has been extensively studied in various animal models, including rodents and other mammals. Fish, such as zebrafish (Danio rerio), have recently emerged as powerful aquatic model organisms with overt individual differences in behavioral, nociceptive and other CNS traits. Here, we evaluate individual behavioral differences in mammals and fish, emphasizing the importance of cross-species analyses of intraspecies variance in experimental models of normal and pathological CNS functions.
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Age-related hearing loss affects the ability to hear high frequencies and therefore leads to difficulties in understanding speech, particularly under adverse listening conditions. This decrease in hearing can be partly compensated by the recruitment of executive functions, such as working memory. The compensatory effort may, however, lead to a decrease in available neural resources compromising cognitive abilities. ⋯ Cognitive flexibility and hearing abilities further predicted speech-in-noise perception. We conclude that neural and behavioral signatures of working memory are intact in mild to moderate hearing loss. Moreover, cognitive flexibility seems to be closely related to hearing impairment and speech-in-noise perception and should, therefore, be investigated in future studies assessing age-related hearing loss and its implications on prefrontal functions.
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Microglia are the brain mononuclear phagocytes which plays a key role in neurodegenerative diseases, like Alzheimer's. Till date, microglia have been explored mostly for their neuro-inflammatory functions. Recent studies have shifted their focus towards less explored functions which involve non-autonomous clearance of protein aggregates. ⋯ Sulforaphane (SFN) treatment has shown to induce the phagocytic activity of Aβo treated microglial cells. In addition, low dose Aβo and SFN treatment have not shown modulation in the levels of pro-inflammatory mediators of microglia. Taken together, these findings suggest that SFN treatment may ameliorate the Aβo mediated decrease in microglial phagocytic activity.
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In this study we used functional MRI (fMRI) to examine whether defining a stimulus as a target affects brain activation associated with a verbal working memory (WM) task. Seventeen healthy right-handed volunteers performed a Sternberg task with three consonants as memory set. We performed a region of interest based fMRI analysis to examine differences in brain activity patterns between targets and non-targets. ⋯ Our results suggest an important hemispheric differentiation in target processing, in which the right frontal cortex is predominantly involved in processes associated with target stimuli. The left frontal cortex does not differentiate between processing target and non-target stimuli, suggesting involvement in WM processes that are independent of stimulus type. Parietal, the lateral anterior part is predominantly involved in target processing, while the medial posterior part does not differentiate between target and non-target processing.
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The primary cause of harmaline tremor, which is a model of essential tremor (ET) in animals, is excessive activation of olivocerebellar glutamatergic climbing fibers. Our recent study indicated that 5'-chloro-5'-deoxy-(±)-N6-(±)-(endo-norborn-2-yl)adenosine (5'Cl5'd-(±)-ENBA), a potent and selective adenosine A1 receptor (A1) agonist, inhibited harmaline tremor. The present study was aimed to evaluate the role of glutamatergic transmission system in 5'Cl5'd-(±)-ENBA tremorolytic action in the harmaline model in rats, by analyzing glutamate release in the motor nuclei of the thalamus and mRNA expression of glutamatergic neuron markers (vGlut1/2) in reference to the general neuronal activity marker (zif-268) in different brain structures. ⋯ The intensity of tremor was measured automatically using Force Plate Actimeters (FPAs). 5'Cl5'd-(±)-ENBA (0.5 mg/kg) given 30 min before harmaline (30 mg/kg) decreased the harmaline-induced excessive glutamate release in the motor thalamus and reversed harmaline-induced molecular effects, such as elevation of the vGlut1 mRNA expression in the inferior olive (IO) and decrease in the motor cortex, as well as an increase of the zif-268 mRNA expression in the IO, motor thalamus and motor cortex. Moreover, 5'Cl5'd-(±)-ENBA reduced harmaline tremor by lowering its power in 9-15 Hz frequency band. Our findings show that A1 stimulation decreases glutamate release in the motor thalamic nuclei in the harmaline model of ET, suggesting that A1 receptors, especially in this structure, may be a potential therapeutic target in this disorder.