Neuroscience
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The fact that neurobiological research is reliant upon laboratory-reared rodents is well known. The following paper discusses this topic broadly, but also aims to highlight other species used in the study of the nervous system and the evolution of animal species usage from the end of World War II through recent investigations. ⋯ Such a limitation in animal species causes many difficulties in the development of new therapies for various neuropsychiatric diseases. Based on numerous scientific publications, the advantages of using a greater diversity of species in neuroscience and the disadvantages of focusing on mice and rats are presented.
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Although the recognition of facial expressions seems automatic and effortless, discrimination of expressions can still be error prone. Common errors are often due to visual similarities between some expressions (e.g., fear and surprise). However, little is known about the neural mechanisms underlying such a confusion effect. ⋯ No difference between high confusion and low confusion conditions was observed on the M170 component in either the FFA or the pSTS, whilst a difference between two conditions started to emerge in the late positive potential (LPP), with the low confusion condition eliciting a larger LPP amplitude in the FFA. In addition, the power of delta was stronger in the time window of LPP component. This confusion effect was reflected in the FFA, which might be associated with the perceptual-to-conceptual shift.
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Parkinson's disease (PD) is caused by neurodegeneration of nigrostriatal neurons, resulting in dopamine (DA) stimulated motor deficits. Like brain derived neurotrophic factor (BDNF), 7,8-dihydroxyflavone (DHF) is an agonist of the tropomyosin receptor kinase-B (TrkB) and stimulates the same secondary cascades that promote neuronal growth, survival and differentiation. We used our progressive mouse model of PD by administering increasing doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) over 4 weeks (5 days/week), and then treated mice with DHF for 4 weeks after the cessation of the toxin injections (i.e., restoration). ⋯ Expression of the sprouting biomarker, superior cervical ganglion 10 (SCG10), was increased ∼20% in the DL striatum and 66% in the SN/midbrain in mice treated with DHF compared to the MPTP only group. We report that after 4 weeks of progressive MPTP administration, DHF can restore motor deficits and TH within the DL striatum in a TrkB-dependent manner. Our data suggests that DHF may help alleviate motor symptoms of PD and restore the loss of DA terminals within the striatum.
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The cerebellum is involved in the coordination of movement. Its cellular composition is dominated by GABAergic neuronal types, and glial cells are known to express functional receptors. GABAergic signaling regulates cell proliferation, differentiation, and migration during neurodevelopment. ⋯ The second population showed an outward-rectifying current-voltage relationship and responded to muscimol, but dye coupling was absent. These cells received synaptic input and were NG2+, but evoked calcium waves failed to modulate the frequency of spontaneous postsynaptic currents (sPSCs) or signaling into NG2 glia. We conclude that GABAA receptor-mediated signaling is selective for NG2 glia in the WM of the cerebellum.
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Mechanisms initiated by traumatic brain injury (TBI), leading to the development of progressive secondary injury are poorly understood. MicroRNAs (miRNAs) have a proposed role in orchestrating the post-injury aftermath as a single miRNA can control the expression of several genes. We hypothesized that the post-injury level of circulating brain-enriched miR-124-3p explains the extent of post-TBI cortical lesion. ⋯ T2-weighted MRI revealed inter-animal differences in cortical lesion area. Linear regression analysis revealed that higher the plasma miR-124-3p level at 2 d post-TBI, larger the lesion area at chronic time point (R2 = 0.327, p < 0.01). Our findings indicate that the extent of lateral fluid-percussion injury-induced chronic cortical pathology associated with the acutely elevated plasma miR-124-3p level.