Brain research
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As accurate finger movements depend on guidance by afferent sensory feedback information, it is of interest to examine how the cortical processing of afferent signals is altered during movement states compared with rest. In the present study we evaluated afferent input to the primary somatosensory cortex (SI) in human subjects performing a finger opposition task. We recorded somatosensory evoked magnetic fields (SEFs) in 6 healthy subjects to stimulation of left and right median nerves in a resting condition and during active right-sided finger movements. ⋯ As the P35m SEF deflection likely represents postsynaptic IPSPs at SI, the results suggest that postsynaptic inhibition to somatosensory impulses from the moving part of the body is suppressed. Comparison of the present results with recent intracellular studies in behaving mice suggests that the P35m reduction specifically corresponds to a reduction in the activity of parvalbumin-containing fast-spiking inhibitory interneurons during movement. The results provide evidence that precision movements can be executed without this type of cortical postsynaptic inhibition.
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β-amyloid (Aβ) aggregates are known to induce neuronal and synaptic dysfunction, and thus are involved in learning and memory deficits in Alzheimer's disease (AD), making Aβ deposits a potential target for prevention or treatment. Microglia, especially bone marrow-derived microglia (BMDM), has been recently thought to play important roles in internalizing and phagocytozing Aβ. BMDM originate in the bone marrow, migrate into the blood as hematopoietic progenitor cells (HPCs) and enter the brain in a chemokine-dependent manner. ⋯ To explore whether treatment with SDF-1α can decrease Aβ burden, APP/PS1 double transgenic mice were given intracerebroventricular injection of SDF-1α weekly from the age of 28 to 32 weeks (4 weeks of injections) or from 28 to 36 weeks (8 weeks of injections). The results of our study showed that SDF-1α treatment decreased the area and the number of Aβ deposits, increased the level of Iba-1, a marker of microglia, and increased the number of plaque associated microglia in the parenchyma of APP/PS1 transgenic mice. These results suggest that SDF-1 could provide a novel and promising target for the purpose of lowering Aβ pathology in AD.
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To investigate whether activation of adenosine A1 receptor (A1R) through limb remote ischemic preconditioning (RIPC) by a noninvasive tourniquet contribute neuroprotective effects against rat focal cerebral ischemic injury induced by transient middle cerebral artery occlusion (MCAO). ⋯ The present study demonstrates that limb RIPC induced by noninvasive tourniquet reduces cerebral ischemic injury in rats, and the effect of neuroprotection may depend on the activation of adenosine A1 receptors. CCPA pretreatment can induce delayed ischemic tolerance against cerebral ischemia/reperfusion injury. These protective effects are associated with a reduction in oxidative stress, inflammation and endogenous antioxidant preservation.
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We investigated optic nerve and geniculocalcarine tract (GCT) in acquired blindness (AB) using routine cranium magnetic resonance imaging and diffusion tensor imaging. Twenty individuals with AB were compared with 20 normally sighted (NS) individuals. The transverse diameters of optic nerves in NS were significantly bigger than the AB participants in T(1)WI maps. ⋯ No diffusion-index alterations in the GCT were found between AB participants and NS controls. White matter integrity remained normal in the GCT. Thus, the GCT may not rely on visual afferent input to maintain integrity after development.