Neuroscience
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Chronic exposure to alcohol produces changes in the prefrontal cortex that are thought to contribute to the development and maintenance of alcoholism. A large body of literature suggests that stress hormones play a critical role in this process. Here we review the bi-directional relationship between alcohol and stress hormones, and discuss how alcohol acutely stimulates the release of glucocorticoids and induces enduring modifications to neuroendocrine stress circuits during the transition from non-dependent drinking to alcohol dependence. We propose a pathway by which alcohol and stress hormones elicit neuroadaptive changes in prefrontal circuitry that could contribute functionally to a dampened neuroendocrine state and the increased propensity to relapse-a spiraling trajectory that could eventually lead to dependence.
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The temporo-parietal (TP) white matter connections between the inferior parietal lobule and superior temporal gyrus as part of the superior longitudinal fasciculus/arcuate fasciculus (SLF/AF) or middle longitudinal fasciculus (MdLF) have been studied in prior diffusion tensor tractography (DTT) studies. However, few studies have been focusing on the higher TP connections of the superior parietal lobule with the temporal lobe. These higher TP connections have been shown to have a role in core processes such as attention, memory, emotions, and language. ⋯ Using a high resolution DTT technique, we demonstrate for the first time, the trajectory of a long fiber bundle connectivity between the SPL and posterior temporal lobe, called the SLF/AF TP-SPL (or the TP-SPL), bilaterally in five healthy adult human brains. We also demonstrate the trajectory of the vertically oriented posterior TP connections, interconnecting the inferior parietal lobule (IPL) with the posterior temporal lobe (TP-IPL) in relation to the TP-SPL, arcuate fasciculus and other major language pathways. In the current study, for the first time, we categorized the TP connections into the anterior and posterior connectivity groups and subcategorized each one into the SPL or IPL connections.
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In vitro studies have demonstrated that β2-adrenergic receptor activation stimulates glycogen degradation in astrocytes, generating lactate as a potential energy source for neurons. Using in vivo microdialysis in mouse cerebellar white matter we demonstrate continuous axonal lactate uptake and glial-axonal metabolic coupling of glutamate/lactate exchange. ⋯ In two-photon imaging experiments on ex vivo mouse corpus callosum subjected to aglycemia, β2-adrenergic activation rescued axons, whereas inhibition of axonal lactate uptake by α-cyano-4-hydroxycinnamic acid (4-CIN) was associated with severe axonal loss. Our results suggest that axonal protective effects of glial β2-adrenergic receptor activation are not mediated by enhanced lactate production.
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Complex molecular and cellular mechanisms regulate G protein-coupled receptors (GPCRs). It is suggested that proteins intrinsically disordered regions (IDRs) are to play a role in GPCR's intra and extracellular regions plasticity, due to their potential for post-translational modification and interaction with other proteins. These regions are defined as lacking a stable three-dimensional (3D) structure. ⋯ About 90% of the receptors had at least one putative site for dimerization in their 3IL or C-terminus. ELM instances sampled in these domains were 14-3-3, SH3, SH2 and PDZ motifs. In conclusion, the increased flexibility observed in GPCRs, added to the enrichment of linear motifs, PEST and heteromerization sites, may be critical for the nervous system's functional plasticity.
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When performing self-paced movements in a fatigued state, internal models can predict the mechanical effects of muscle fatigue. Yet, it is unclear if this is still true when movements are submitted to additional constraints. The purpose of the present study was to investigate the Central Nervous System's (CNS) capacity to integrate fatigue signals into forward models' prediction processes when the movement to perform is unpredictable and temporally constrained. ⋯ While the fatigue protocol resulted in significant alterations of arm flexion peak accelerations, APAs were not modified post-fatigue as compared to control trials. It is proposed that with unpredictable and temporally constrained movements, the CNS cannot incorporate fatigue signals in internal models' prediction processes to reweight the motor information contained in the efference copy. It is also suggested that APA implementation is based on predictive processes occurring in internal models located upstream from M1.