Neuroscience
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In this study, we analyzed the spatiotemporal alterations of phospholipid composition in the spinal cord of an amyotrophic lateral sclerosis (ALS) mouse model (G93A-mutated human superoxide dismutase 1 transgenic mice [SOD1(G93A) mice]) using imaging mass spectrometry (IMS), a powerful method to visualize spatial distributions of various types of molecules in situ. Using this technique, we deciphered the phospholipid distribution in the pre-symptomatic stage, early stage after disease onset, and terminal stages of disease in female SOD1(G93A) mouse spinal cords. These experiments revealed a significant decrease in levels of docosahexaenoic acid (DHA)-containing phosphatidylcholines (PCs), such as PC (diacyl-16:0/22:6), PC (diacyl-18:0/22:6), and PC (diacyl-18:1/22:6) in the L5 anterior horns of terminal stage (22-week-old) SOD1(G93A) mice. ⋯ Thus, our study showed a significant decrease in DHA-containing PCs, but not other PCs, in the terminal stage of ALS in model mice, which is likely to be a reflection of neuronal loss in the anterior horns of the spinal cords. Given its enrichment in dorsal sensory regions, the preservation of PC (diacyl-16:0/16:0) may be the result of spinal sensory neurons being unaffected in ALS. Taken together, these findings suggest that ALS spinal cords show significant alterations in PC metabolism only at the terminal stage of the disease, and that these changes are confined to specific anatomical regions and cell types.
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Converging evidences suggest that mental movement simulation and actual movement production share similar neurocognitive and learning processes. Although a large body of data is available in the literature regarding mental states involving the dominant arm, examinations for the nondominant arm are sparse. Does mental training, through motor-imagery practice, with the dominant arm or the nondominant arm is equally efficient for motor learning? In the current study, we investigated laterality effects in motor learning by motor-imagery practice. ⋯ No such improvements were observed in the control group. Our results suggest a superiority of the dominant arm in motor learning by mental practice. We discussed these findings from the perspective of the internal models theory.
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We investigated the role of the autonomic nervous system to cardiovascular responses to obstructive apnea in awake, unrestrained rats, and measured expression of Fos induced by apnea in the brainstem. We implanted a tracheal balloon contained in a rigid tube to allow the induction of apnea without inducing pain in the trachea. During bouts of 15s of apnea, heart rate fell from 371±8 to 161±11bpm (mean±SEM, n=15, p<0.01) and arterial pressure increased from 115±2 to 131±4mmHg (p<0.01). ⋯ Apnea induced Fos expression in several brainstem areas involved in cardiorespiratory control such as the nucleus of the solitary tract (NTS), ventrolateral medulla (VLM), and pons. Ligation of the carotid body artery reduced apnea-induced bradycardia, blocked heart rate responses to i.v. injection of cyanide, reduced Fos expression in the caudal NTS, and increased Fos expression in the rostral VLM. In conclusion, apnea activates neurons in regions that process signals from baroreceptors, chemoreceptors, pulmonary receptors, and regions responsible for autonomic and respiratory activity both in the presence and absence of carotid chemoreceptors.
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Fibronectin type III domain containing 5 (Fndc5) has already been distinguished to be involved in neural differentiation. However, cellular events of Fndc5 function are still ambiguous in the nervous system. One approach to shed light on duty of this protein in the nervous system is to find its cross-talks with various signaling pathways with defined characteristics and roles. ⋯ Furthermore, inhibition of this pathway by PD0325901 dramatically reduced Fndc5 mRNA level, while activating the pathway up-regulated Fndc5 transcription. In addition, it has been proven that ERK1/2 modulation via RA has more significant controlling effect on Fndc5 promoter rather than bFGF. This led us to conclude that RA enhances Fndc5 expression through a non-genomic pathway via the ERK signaling pathway.
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Recent studies have demonstrated that inflammatory and immune mechanisms play important roles in the progression of chronic cerebral hypoperfusion (CCH)-induced white matter lesions (WMLs). As an endogenous neuromodulator in the brain, the extracellular levels of adenosine represent a critical endogenous mechanism for the regulation of immune and inflammatory responses. Ecto-5'-nucleotidase (CD73), which dephosphorylates AMP to adenosine, is considered to catalyze the rate-limiting step in the generation of extracellular adenosine. ⋯ More reactive astrocytes and microglia were observed in the corpus callosum in CD73-KO mice. CD73 deficiency significantly increased the levels of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in the BCAS model of CCH. These findings suggest that CD73 plays a protective role in the development of CCH-induced WMLs and cognitive impairment via the regulation of glial cell activation and proinflammatory cytokine expression.