Cerebral cortex
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Comparative Study
Unique contributions of distinct cholinergic projections to motor cortical plasticity and learning.
The cholinergic basal forebrain projects throughout the neocortex, exerting a critical role in modulating plasticity associated with normal learning. Cholinergic modulation of cortical plasticity could arise from 3 distinct mechanisms by 1) "direct" modulation via cholinergic inputs to regions undergoing plasticity, 2) "indirect" modulation via cholinergic projections to anterior, prefrontal attentional systems, or 3) modulating more global aspects of processing via distributed inputs throughout the cortex. To segregate these potential mechanisms, we investigated cholinergic-dependent reorganization of cortical motor representations in rats undergoing skilled motor learning. ⋯ Global cholinergic depletion perturbs map plasticity comparable with motor cortex depletions but results in significantly greater impairments in skilled motor acquisition. These findings indicate that local cholinergic activation within motor cortex, as opposed to indirect regulation of prefrontal systems, modulate cortical map plasticity and motor learning. More globally acting cholinergic mechanisms provide additional support for the acquisition of skilled motor behaviors, beyond those associated with cortical map reorganization.
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Evidence shows that administration of D-galactose (D-gal) induces reactive oxygen species (ROS) production and inflammatory response resulting in neurodegenerative changes. Ursolic acid (UA), a triterpenoid compound, has been reported to possess antioxidant and anti-inflammatory properties. Our previous studies have demonstrated that UA could protect mouse brain against D-gal-induced oxidative damage. ⋯ Furthermore, the results also showed that UA significantly reduced the number of activated microglia cells and astrocytes, decreased the expression of CD11b and glial fibrillary acidic protein, downregulated the expression of iNOS and COX-2, and decreased interleukin (IL)-1β, IL-6, and tumor necrosis factor-α levels in the prefrontal cortex of D-gal-treated mice. Moreover, UA significantly decreased AGEs induced the expression of receptor for advanced glycation end products and inhibited NF-κB p65 nuclear translocation in the prefrontal cortex of D-gal-treated mice. The aforementioned effects of UA could attenuate brain inflammatory response.