Neuroscience
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We have recently shown that folate deficiency induces depression-like behavior and neuronal immaturity in the dentate gyrus (DG) in mice. We also revealed that folate deficiency inhibits neuronal maturation, hypomethylates the promoter of certain neuronal genes and decreases intracellular levels of S-adenosylmethionine (SAM), a methyl donor, in cultured neural stem and progenitor cells. Based on these findings, we hypothesized that SAM reduction may be involved in a folate deficiency-induced depressive state and neural immaturity. ⋯ Furthermore, neurofunctional and neuromorphological abnormalities in the DG of low folate diet-fed mice, such as decreases in stress-induced expression of c-Fos (a neuronal activity marker), dendritic complexity and the number of mature spines, were improved by SAM supplementation. The disrupted expression of transcription factors involved in neuronal differentiation and maturation was also normalized by SAM supplementation. These results suggest that SAM reduction may be involved in a folate deficiency-induced depressive state.
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Large cholinergic neurons (V0c neurons; aka, partition cells) in the spinal cord project profusely to motoneurons on which they form C-terminal contacts distinguished by their specialized postsynaptic subsurface cisterns (SSCs). The V0c neurons are known to be rhythmically active during locomotion and release of acetylcholine (ACh) from their terminals is known to modulate the excitability of motoneurons in what appears to be a task-dependent manner. Here, we present evidence that a subpopulation of V0c neurons express the gap junction forming protein connexin36 (Cx36), indicating that they are coupled by electrical synapses. ⋯ We present evidence that fast vs. slow motoneurons have a greater abundance of these terminals and fast motoneurons also have the highest density that were eGFP+. Thus, our results indicate that a subpopulation of V0c neurons projects preferentially to fast motoneurons, suggesting that the capacity for synchronous activity conferred by electrical synapses among networks of coupled V0c neurons enhances their dynamic capabilities for synchronous regulation of motoneuron excitability during high muscle force generation. The eGFP+ vs. eGFP- V0c neurons were more richly innervated by serotonergic terminals, suggesting their greater propensity for regulation by descending serotonergic systems.
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The primary motor cortex, a dynamic center for overall motion control and decision making, undergoes significant alterations upon neural stimulation. Over the last few decades, data from numerous studies using rodent models have improved our understanding of the morphological and functional plasticity of the primary motor cortex. ⋯ However, whether the modifications of specific synapses are associated with motor learning should be studied further. In this review, we summarized the findings of prior studies on the features and dynamics of the primary motor cortex in rodents.
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Aging is associated with altered brain connectivity within the default mode network (DMN). Although research using functional magnetic resonance imaging has quantified age-related alterations in functional connectivity within this network during resting state, it is less clear how this may be reflected in electrophysiological measures, and how this relates to cognitive performance in older adults. The aim of this study was to quantify age differences in phase synchrony of the DMN during resting state, with particular focus on connectivity between the anterior node (i.e., medial prefrontal cortex, or mPFC) and other associated regions in this network. ⋯ Findings indicated decreased connectivity in the alpha2 range for older than younger adults between the mPFC and other DMN regions including the left angular gyrus and bilateral lateral temporal cortices, the latter of which were associated with lower performance in semantic fluency and executive functioning in older adults. Furthermore, greater PLV in theta and beta bands between the mPFC and posterior cingulate regions were found in older than younger adults. These results suggest age-related changes in DMN functional connectivity are non-uniform and frequency-dependent, and may reflect poorer performance in cognitive domains thought to decline with aging.
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Afferent inputs to the primary somatosensory cortex (S1) are differentially processed during precision and power grip in humans. However, it remains unclear how S1 interacts with the primary motor cortex (M1) during these two grasping behaviors. To address this question, we measured short-latency afferent inhibition (SAI), reflecting S1-M1 interactions via thalamo-cortical pathways, using paired-pulse transcranial magnetic stimulation (TMS) during precision and power grip. ⋯ The M1 receives movement information from S1 through direct cortico-cortical pathways, so intra-hemispheric S1-M1 interactions using dual-site TMS were also evaluated. Stimulation of S1 attenuated M1 excitability (S1-M1 inhibition) during precision and power grip, while the S1-M1 inhibition ratio remained similar across tasks. Taken together,our findings suggest that distinct neural mechanisms for S1-M1 interactions mediate precision and power grip, presumably by modulating neural activity along thalamo-cortical pathways.