Neuroscience
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Numerous studies have reported that the hippocampus in schizophrenia patients is reduced in volume compared to the normal population. Antipsychotic medications have had mixed benefits in maintaining hippocampal volume or reversing volume loss. Recent evidence indicates that routine aerobic exercise represents a promising intervention for reversing hippocampal loss and cognitive deficits. ⋯ The hippocampal sub-regions of the dentate gyrus and CA1 were most strongly affected by olanzapine and exercise. Of interest, there was a strong and highly significant negative correlation between glucose intolerance and hippocampal volume, whereby greater glucose intolerance was associated with a smaller hippocampal volume. These findings indicate that exercise may have beneficial effects on the hippocampus when antipsychotic medication can contribute to changes in volume.
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Clinical stimulation of preterm infant breathing with methylxanthines like caffeine and theophylline can evoke seizures. It is unknown whether underlying neuronal hyperexcitability involves the rhythmogenic inspiratory active pre-Bötzinger complex (preBötC) in the brainstem or preBötC-driven motor networks. Inspiratory-related preBötC interneuronal plus spinal (cervical/phrenic) or cranial hypoglossal (XII) motoneuronal bursting was studied in newborn rat en bloc brainstem-spinal cords and brainstem slices, respectively. ⋯ Methylxanthines (2.5-10mM), but not blockade of adenosine receptors, phosphodiesterase-4 or the sarcoplasmatic/endoplasmatic reticulum ATPase countered inspiratory depression by muscimol-evoked GABAA receptor activation that was associated with a hyperpolarization and input resistance decrease silencing preBötC neurons in slices. The latter blockers did neither affect preBötC or cranial/spinal motor network bursting nor evoke seizure-like activity or mask corresponding methylxanthine-evoked discharges. Our findings show that methylxanthine-evoked hyperexcitability originates from motor networks, leaving preBötC activity largely unaffected, and suggest that GABAA receptors contribute to methylxanthine-evoked seizure-like perturbation of spinal motoneurons whereas non-respiratory XII motoneuron oscillations are of different origin.
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Most investigations into the role of the body axis in vertebrate locomotion have focused on the trunk, although in most tetrapods, the tail also plays an active role. In salamanders, the tail contributes to propulsion during swimming and to dynamic balance and maneuverability during terrestrial locomotion. The aim of the present study was to obtain information concerning the neural mechanisms that produce tail muscle contractions during locomotion in the salamander Pleurodeles waltlii. ⋯ Together, our results demonstrate the existence of a pattern generator for rhythmic tail movements in the salamander and show that the global architecture of the tail network is similar to that previously proposed for the mid-trunk locomotor network in the salamander. Our findings further support the view that salamanders can control their trunk and tail independently during stepping movements. The relevance of our results in relation to the generation of tail muscle contractions in freely moving salamanders is discussed.
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Neonatal hypoxia-ischemic encephalopathy (HIE) remains a major cause of brain damage, leading to high disability and mortality rates in neonates. In vitro studies have shown that hesperidin, a flavanone glycoside found abundantly in citrus fruits, acts as an antioxidant. Although hesperidin has been considered as a potential treatment for HIE, its effects have not been fully evaluated. ⋯ The neuroprotective effects of hesperidin are likely the results of preventing an increase in intracellular reactive oxygen species and lipid peroxide levels. Hesperidin treatment also activated a key survival signaling kinase, Akt, and suppressed the P-FoxO3 level. Hesperidin pretreatment protected neonatal HIE by reducing free radicals and activating phosphorylated Akt.
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Aged ovariectomized (OVX) female monkeys, a model for menopause in humans, show a decline in spine density in the dorsolateral prefrontal cortex (dlPFC) and diminished performance in cognitive tasks requiring this brain region. Previous studies in our laboratory have shown that long-term cyclic treatment with 17β-estradiol (E) produces an increase in spine density and in the proportion of thinner spines in layer III pyramidal neurons in the dlPFC of both young and aged OVX rhesus monkeys. Here we used 3D reconstruction of Lucifer yellow-loaded neurons to investigate whether clinically relevant schedules of hormone therapy would produce similar changes in prefrontal cortical neuronal morphology as long-term cyclic E treatment in young female monkeys. ⋯ When compared with the results of our previously published investigations, our results suggest that cyclic fluctuations in serum E levels may cause corresponding fluctuations in the density of thin spines in the dlPFC. By contrast, continuous administration of E does not support sustained increases in thin spine density. Physiological fluctuations in E concentration may be necessary to maintain the morphological sensitivity of the dlPFC to E.