Neuroscience letters
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Neuroscience letters · Aug 2011
BDNF and GAP43 contribute to dynamic transhemispheric functional reorganization in rat brain after contralateral C7 root transfer following brachial plexus avulsion injuries.
It is known that contralateral seventh cervical nerve (C7) root transfer after brachial plexus avulsion injuries (BPAI) causes interhemispheric cortical functional reorganization. However, the potential mechanisms and the role of neurotrophic factors and/or growth-associated protein expression in the process of cerebral reorganization are not well understood. ⋯ BDNF and GAP43 mRNA levels were significantly increased in brain samples at both 6 and 9 months after contralateral C7 root transfer following BPAI, in comparison with the samples from the rats with BPAI only. These findings indicate that BDNF and GAP43 may play an important role during the dynamic transhemispheric functional reorganization.
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Neuroscience letters · Jul 2011
AMP-activated protein kinase activates neuropeptide Y neurons in the hypothalamic arcuate nucleus to increase food intake in rats.
AMP-activated protein kinase (AMPK) is an energy sensor that is activated by the increase of intracellular AMP:ATP ratio. AMPK in the hypothalamic arcuate nucleus (ARC) is activated during fasting and the activation of AMPK stimulates food intake. To clarify the pathway underlying AMPK-induced feeding, we monitored the activity of single ARC neurons by measuring cytosolic Ca(2+) concentration ([Ca(2+)](i)) with fura-2 fluorescence imaging. ⋯ Intracerebroventricular administration of AICAR increased food intake, and the AICAR-induced food intake was abolished by the co-administration of NPY Y1 receptor antagonist, 1229U91. These results indicate that the activation of AMPK leads to the activation of ARC NPY neurons through Ca(2+) influx, thereby causing NPY-dependent food intake. These mechanisms could be implicated in the stimulation of food intake by physiological orexigenic substances.
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Neuroscience letters · Jul 2011
Comparative StudyLesions of the dentate and interposed nuclei are associated with impaired prehension in cerebellar patients.
In a recent study using voxel based lesion symptom mapping (VLSM) in cerebellar patients following stroke we found associations of prehensile deficits to lesions of the cerebellar cortex and dentate nucleus (DN). Associations to lesions of the interposed nucleus (IN), which has been shown to contribute to prehension in monkeys, could not be established. One possible reason was that the IN was largely unaffected in the stroke patients. ⋯ These were associated with lesions of the intermediate and lateral cerebellar cortex together with their output nuclei. Specifically, IN lesions were linked to increased lift-off time in grasping and not to slower reaching movements. Thus, our data support IN contribution particularly for the fluent production of grip forces during dexterous prehension in humans.
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Neuroscience letters · Jul 2011
Comparative StudyMale Internet addicts show impaired executive control ability: evidence from a color-word Stroop task.
This study investigated the executive control ability of male students with Internet addiction disorder (IAD) by recording event-related brain potentials (ERP) during a color-word Stroop task. Seventeen IAD and 17 male normal university students participated. ⋯ ERP results revealed that participants with IAD showed reduced medial frontal negativity (MFN) deflection in incongruent conditions than the control group. Both of the behavioral performance and ERP results indicate that people with IAD show impaired executive control ability than the normal group.
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Neuroscience letters · Jul 2011
Post-learning REM sleep deprivation impairs long-term memory: reversal by acute nicotine treatment.
Rapid eye movement sleep deprivation (REM-SD) is associated with spatial learning and memory impairment. During REM-SD, an increase in nicotine consumption among habitual smokers and initiation of tobacco use by non-smokers have been reported. We have shown recently that nicotine treatment prevented learning and memory impairments associated with REM-SD. ⋯ However, nicotine treatment reversed the post-learning REM-SD-induced impairment of long-term memory. On the other hand, post-learning treatment of normal rats with nicotine for 24h enhanced long-term memory. These results indicate that post-learning acute nicotine treatment prevented the deleterious effect of REM-SD on cognitive abilities.