Neuroscience
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This study was designed to examine the effects of chronic running exercise (Ex) on the hypobaric hypoxia-induced neuronal injury in the hippocampus. Male Wistar rats (9 weeks old) were caged in a hypoxic altitude chamber simulating the condition of 9,000 m high (0.303 atm) for 7h and the brains were examined at 0, 4, and 24h after treatment. Hypoxia challenge increased the levels of caspase 3 (mean ± SEM, % of baseline control, 121.9 ± 11.8, 152.3 ± 15.3, 141.6 ± 7.0 for 0, 4 and 24h, respectively, n=5) and induced apoptosis (cell number, 205.7 ± 8.8, 342.3 ± 33.4, 403.0 ± 12.2 for 0, 4 and 24h vs. 7.7 ± 1.4 baseline control, n=3) in the hippocampal CA1 pyramidal neurons. ⋯ Taken together, our results show that chronic Ex protects hippocampal CA1 neurons against hypobaric hypoxia insult. Ex-enhanced bioenergetic adaptation and anti-oxidative capacity may prevent neurons from hypoxia-induced apoptosis. Furthermore, activation of the BDNF signaling pathway may be involved in the Ex-induced protection.
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In adult mammals, newborn neural precursor cells (NPCs) derived from either the subventricular zone (SVZ) or the subgranular zone (SGZ) migrate into the olfactory bulb and the dentate gyrus (DG), respectively, where some of them mature into excitatory and inhibitory neurons. There is increasing evidence that this neurogenesis process is important for some types of learning and synaptic plasticity and vice versa. Survivin, a member of the inhibitor-of-apoptosis protein (IAP) family, has been suggested to have a central role in the regulation of neurogenesis. ⋯ Here we examined adult Survivin(Camcre) mice with a conditional deletion of the survivin gene in embryonic neurogenic regions. Although the deletion of survivin had no effect on basic excitability in DG and CA1-region, there was a marked impairment of long-term potentiation (LTP) in these areas. Our data support a function of survivin in hippocampal synaptic plasticity and learning and underline the importance of adult brain neurogenesis for proper operation of the hippocampal tri-synaptic circuit and the physiological functions that depend on it.
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Adderall is widely prescribed for attention deficit hyperactivity disorder (ADHD) though long term neurological effects of the main ingredient d-amphetamine are not well understood. The purpose of this study was to examine effects of clinically prescribed doses of d-amphetamine and one abuse dose administered from childhood to adulthood on adult hippocampal neurogenesis and activation of the granule layer of the dentate gyrus. Beginning in early adolescence (age 28 days) to adulthood (age 71), male C57BL/6J mice were administered twice daily i.p. injections of vehicle, 0.25, 0.5 or 2mg/kg d-amphetamine. ⋯ Results suggest both therapeutic and abuse doses of d-amphetamine increase the number of new neurons in the hippocampus when administered from adolescence to adulthood by increasing survival and differentiation of cells into neurons not by increasing progenitor cell proliferation. Mechanisms for amphetamine-induced neurogenesis are unknown but appear activity independent. Results suggest part of the beneficial effects of therapeutic doses of d-amphetamine for ADHD could be via increased hippocampal neurogenesis.
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The relationship between learning/memory performance and long-term potentiation (LTP) induction is ambiguous. Although a large body of data supports a strong correspondence between learning/memory performance and LTP, many studies have also provided evidence to the contrary. In this study, we found that 2-month-old senescence-accelerated mice/prone 8 (SAMP8 mice) displayed both impaired performance in a Morris Water Maze (MWM) and enhanced LTP compared to senescence-accelerated mice/resistance 1 (SAMR1). ⋯ Further analysis demonstrated that the increase in cytokine content was higher in the hippocampal tissues used for LTP recording in the SAMR1 and CFA-challenged animals compared to the SAMP8 and intact BALB/c mice. A correlation analysis demonstrated that pro-inflammatory cytokines (IL-6 and TNF-α) displayed a negative correlation with LTP, while an anti-inflammatory cytokine (IL-10) displayed a positive correlation with LTP. These results suggest that pro-inflammatory cytokines induced by LTP manipulation in experiments (e.g., via tissue injury caused by electrode insertion) may be one of the factors contributing to the observed lack of correspondence between memory/learning ability and LTP.
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Biofeedback training is an efficient means to gain control over a physiological function typically considered involuntary. Accordingly, learning to self-regulate nociceptive physiological activity may improve pain control by activating endogenous modulatory processes. The aim of the present study was to assess whether trial-by-trial visual feedback of nociceptive flexion reflex (RIII-reflex) responses (an index of spinal nociception) evoked by brief painful shocks applied to the sural nerve could be beneficial to guide participants in adopting strategies aiming at modulating pain perception. ⋯ The biofeedback group was not significantly superior to the sham and the control groups in the modulation of RIII-reflex amplitude, pain intensity or unpleasantness. These results are consistent with the notion that RIII-reflex amplitude and pain perception can be modulated voluntarily by various cognitive strategies. However, immediate retrospective visual feedback of acute nociceptive responses presented iteratively in successive trials may not improve the efficacy of these self-regulation processes.