Neuroscience
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Previous studies yielded evidence for an interaction between age and valence in numerous cognitive processes. But, to date, no research has been conducted in the field of motor skills. In this study, we examined the age-related differences in the organization of an emotionally goal-directed locomotion task. ⋯ The fastest RTs were found in younger adults when faced with pleasant pictures, suggesting that older people may focus either on intermediate or final goals, depending on their value of pleasantness, and prioritize positive goals. We also found that the spatial coding of locomotion (trajectory and final body position) was affected in the same way by the valence of the intermediate goal in both age groups. Taken together, these findings provide new perspectives regarding the potential role of the emotional valence of the intermediate and final goals on the cognitive processes involved in action coding, such as in mental representations of action in older adults.
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Creatine, a compound that is critical for energy metabolism of nervous cells, crosses the blood-brain barrier (BBB) and the neuronal plasma membrane with difficulty, and only using its specific transporter. In the hereditary condition where the creatine transporter is defective (creatine transporter deficiency) there is no creatine in the brain, and administration of creatine is useless lacking the transporter. The disease is severe and incurable. ⋯ Finally, creatine gluconate was superior to creatine in increasing tissue content of creatine after transporter block and slowed down PS disappearance during anoxia, an effect that creatine did not have. These findings suggest that coupling creatine to molecules having a specific transporter may be a useful strategy in creatine transporter deficiency. In particular, creatine ascorbate has effects comparable to those of creatine in normal conditions, while being superior to it under conditions of missing or impaired creatine transporter.
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Nonsynaptic mechanism changes, particularly the enhancement of NKCC1 expression in the dentate gyrus (DG) after 4weeks of ethanol consumption, motivate the present work, in which rats were submitted to a period of chronic consumption (12weeks). Four groups of six animals (6-week-old male Wistar rats) were formed, including the control (C), ethanol 1 (E1), ethanol 2 (E2) and ethanol 3 (E3) groups. The rats in the E1, E2 and E3 groups were treated daily with a 30% v/v solution of ethanol, administered via oral gavage (1.0, 2.0 and 3.0g/kg, respectively). ⋯ Confocal microscopy images indicate the NKCC1 increase was pronounced in the initial axonal segment of granule cells. The blockage of these cotransporters during NEA induction with bumetanide suppressed the DC shift increase and diminished all parameters of NEA that were quantified for all groups treated with ethanol. Therefore, the increase in NKCC1 expression and the effective activity of this cotransporter, which were observed in the treated groups, suggest that drugs that act for block NKCC1 represent promising strategies for diminishing the effects of alcohol damage on the brain.
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Blast exposure can cause tinnitus and hearing impairment by damaging the auditory periphery and direct impact to the brain, which trigger neural plasticity in both auditory and non-auditory centers. However, the underlying neurophysiological mechanisms of blast-induced tinnitus are still unknown. ⋯ We also observed an increased bursting rate in the low-frequency region at one month after blast exposure and in all frequency regions at three months after exposure. Taken together, spontaneous firing and bursting activity in the AC played an important role in blast-induced chronic tinnitus as opposed to acute tinnitus, thus favoring a bottom-up mechanism.
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Deregulation of glutamate homeostasis is associated with degenerative neurological disorders. Glutamate dehydrogenase (GDH) is important for glutamate metabolism and plays a central role in expanding the pool of tricarboxylic acid (TCA) cycle intermediate alpha-ketoglutarate (α-KG), which improves overall bioenergetics. Under high energy demand, maintenance of ATP production results in functionally active mitochondria. ⋯ We also found that beta-lapachone increased glutamate utilization, accompanied by a reduction in extracellular glutamate. Thus, our hypothesis that mitochondrial GDH activators increase α-KG production as an alternative energy source for use in the TCA cycle under energy-depleted conditions was confirmed. Our results suggest that increasing GDH-mediated glutamate oxidation represents a new therapeutic intervention for neurodegenerative disorders, including stoke.