Neuroscience
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Orexin neurons are known to augment the sympathetic control of cardiovascular function, however the role of orexin neurons in parasympathetic cardiac regulation remains unclear. To test the hypothesis that orexin neurons contribute to parasympathetic control we selectively expressed channelrhodopsin-2 (ChR2) in orexin neurons in orexin-Cre transgenic rats and examined postsynaptic currents in cardiac vagal neurons (CVNs) in the dorsal motor nucleus of the vagus (DMV). ⋯ These responses were heterogeneous and included excitatory glutamatergic (63%) and inhibitory GABAergic (37%) postsynaptic currents. The results from this study suggest different sub-population of orexin neurons may exert diverse influences on brainstem CVNs and therefore may play distinct functional roles in parasympathetic control of the heart.
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Compared to isometric activities, the neural basis of fatigue induced by repetitive tasks has been scarcely studied. Recently, we showed that during short-lasting repetitive tasks at the maximal possible rate (finger tapping for 10 and 30s), tapping rate and maximal voluntary contraction (MVC) force decrease at the end of finger tapping. We also observed larger silent periods (SP) induced by transcranial magnetic stimulation during MVC post finger tapping. ⋯ While indices of excitability increased initially in both tasks, they decreased with the isometric task only when the task was prolonged to 30s. We suggest that the inability to maintain increased levels of spinal excitability during task execution is a neurophysiological mark of fatigue. Our results suggest that the origin of fatigue induced by brief and fast repetitive tasks is not spinal.
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Vitamin B12 and n-3 polyunsaturated fatty acid (n-3 PUFA) are known to influence cognition. This study aims to examine if these nutrients affect the protein levels and gene expression of nerve growth factor (NGF) and vascular endothelial growth factor (VEGF) in the cortex and hippocampus in the second-generation offspring at 3 mo of age. Wistar rats were fed the following diets for two generations: Control (CON), vitamin B12 deficient (VBD), vitamin B12 deficient supplemented with n-3 PUFA (VBDO), vitamin B12 supplemented (VBS), vitamin B12 supplemented with n-3 PUFA (VBSO). ⋯ However, the VBSO group demonstrated higher (P⩽0.05) NGF gene expression and protein levels in the hippocampus and higher cortex NGF protein levels as compared to the CON group. In addition, VEGF (in hippocampus) and NGF (in cortex and hippocampus) protein levels were also higher (P⩽0.05) in the VBSO group as compared to the VBS group. Our results indicate that the combined supplementation of vitamin B12 and n-3 PUFA improves NGF and maintains VEGF levels in the brain which may improve neurovascular function.
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It is known that anxiety (ANX) impairs action-perception coupling. This study tests whether this impairment could be associated with an alteration of the sensorimotor function. To this aim, the cortical activities underlying the sensorimotor function were recorded in twelve volunteers in a reach-to-grasp paradigm, in which the level of ANX and the position of a glass were manipulated. ⋯ Fast-α-EEG desynchronization was reduced under breath-restriction (-37.7%; p<0.05). The results confirm that ANX-related impairment of action-perception coupling co-modulates with theta-sensorimotor rhythm. This finding is discussed as an altered "readiness state" in the reaching-related cortical network, while individuals are anxious.
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Spinocerebellar ataxia type-3 (SCA-3) is a rare disease but it is the most frequent type within the autosomal dominant inherited ataxias. The disease lacks an effective treatment to alleviate major symptoms and to modify disease progression. Our recent findings that endocannabinoid receptors and enzymes are significantly altered in the post-mortem cerebellum of patients affected by autosomal-dominant hereditary ataxias suggest that targeting the endocannabinoid signaling system may be a promising therapeutic option. ⋯ We also measured the levels of endocannabinoid lipids and found reductions in anandamide and oleoylethanolamide in the brainstem. These changes correlated with an increase in the FAAH enzyme in the brainstem, which also occurred in some cerebellar areas, whereas other endocannabinoid-related enzymes were not altered. Collectively, our results in SCA-3 mutant mice confirm a possible dysregulation in the endocannabinoid system in the most important brain structures affected in this type of ataxia, suggesting that a pharmacological manipulation addressed to correct these changes could be a promising option in SCA-3.