Neuroscience
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Exercise is increasingly being used as a treatment for alcohol use disorders (AUD), but the interactive effects of alcohol and exercise on the brain remain largely unexplored. Alcohol damages the brain, in part by altering glial functioning. In contrast, exercise promotes glial health and plasticity. ⋯ Furthermore, computational arbor analytics revealed that the binged animals (regardless of exercise) had microglia with thicker, shorter arbors and significantly less branching, suggestive of partial activation. We found no changes in the number or morphology of mPFC astrocytes. We conclude that binge alcohol exerts a prolonged effect on morphology of mPFC microglia and limits the capacity of exercise to increase their numbers.
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Perceiving and reproducing direction of visual stimuli in 2-D space produces the visual oblique effect, which manifests as increased precision in the reproduction of cardinal compared to oblique directions. A second cognitive oblique effect emerges when stimulus information is degraded (such as when reproducing stimuli from memory) and manifests as a systematic distortion where reproduced directions close to the cardinal axes deviate toward the oblique, leading to space expansion at cardinal and contraction at oblique axes. We studied the oblique effect in 3-D using a virtual reality system to present a large number of stimuli, covering the surface of an imaginary half sphere, to which subjects had to reach. ⋯ A visual oblique effect was observed for the reproduction of cardinal directions compared to oblique, which did not differ with memory condition. A cognitive oblique effect also emerged, which was significantly larger in the memory compared to the no-memory condition, leading to distortion of directional space with expansion near the cardinal axes and compression near the oblique axes on the hemispherical surface. This effect provides evidence that existing models of 2-D directional space categorization could be extended in the natural 3-D space.
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The prefrontal cortex (PFC) plays a key role in cognitive functions, memory, and attention. Alterations in parvalbumin interneurons (PV neurons) and perineuronal nets (PNNs) within the PFC have been implicated in schizophrenia and autism spectrum disorder pathology. However, it remains unclear why PV neurons and PNNs in the PFC are selectively impaired. ⋯ In the mature PFC, the expression of PV protein is lower than in other parts of the cortex. Furthermore, PNNs in the mature PFC are not typical lattice-like structures and do not have the major components of PNNs and tenascin-R. The present study indicates that PV neurons and PNNs have region-specific features, and our results suggest that PV neurons and PNNs have structural vulnerability within the PFC.
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This review addresses the fundamental question of how we first experience pain, at the beginning of our lives. The brain is activated by peripheral tissue damaging stimulation from birth, but unlike other sensory systems, the pain system in healthy individuals cannot rely upon prolonged activity-dependent shaping through repeated noxious stimulation. Considering the importance of pain, remarkably little is known about when and how nociceptive cortical network activity characteristic of the mature adult brain develops. ⋯ Since this developing brain connectome is necessary, if not sufficient, for pain experience, we discuss the structural and functional development of cortical and subcortical networks that contribute to this network. We then review specific information on the development of nociceptive processing in the infant brain, considering evidence from neurophysiological and hemodynamic measures separately, as the two are not always consistent. Finally we highlight areas that require further research and discuss how information gained from laboratory animal models will greatly increase our understanding in this area.
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Opioids produce strong analgesia but their use is limited by a paradoxical hypersensitivity named opioid-induced hyperalgesia (OIH) that may be associated to analgesic tolerance. In the last decades, a significant number of preclinical studies have investigated the factors that modulate OIH development as well as the cellular and molecular mechanisms underlying OIH. Several factors have been shown to influence OIH including the genetic background and sex differences of experimental animals as well as the opioid regimen. ⋯ Neurons and glial cells exert synergistic effects, which contribute to OIH. The molecular actors identified include the Toll-like receptor 4 and the anti-opioid systems as well as some other excitatory molecules, receptors, channels, chemokines, pro-inflammatory cytokines or lipids. This review summarizes the intracellular and intercellular pathways involved in OIH and highlights some mechanisms that may be challenged to limit OIH in the future.