Neuroscience
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Responses to personal space (PS) violations are variable and depend (besides many other factors) on the sex of the person who enters this space. The neuronal basis of this effect is still largely unknown. A previous neuroimaging investigation had shown that male participants responded with increased amygdala activation to PS violation, but only when the intruder was male. ⋯ When the approaching person was male additional amygdala activation was detected. Because the amygdala is a central structure for the initiation of defense responses, the heightened activation might reflect that male intrusion was decoded as potential threat. Hence, we observed a similar gender bias to simulated space intrusion in women as previously in men.
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The mammalian brain has evolved in close synchrony with the natural environment; consequently, trends toward disengagement from natural environments in today's industrialized societies may compromise adaptive neural responses and lead to psychiatric illness. Investigations of rodents housed in enriched environments indicate enhanced neurobiological complexity; yet, the origin of these stimuli, natural vs. manufactured, has not been sufficiently explored. In the current study, groups of rats were exposed to one of three environments: (1) a standard environment with only food and water, (2) an artificial-enriched environment with manufactured stimuli and (3) a natural-enriched environment with natural stimuli. ⋯ Both enriched groups exhibited less anxiety in response to a novel object but the natural-enriched rats exhibited less anxiety-typical behavior in response to a predator odor than the other groups. Less fos activation in the amygdala was observed in both enriched groups following a water escape task whereas an increase in fos activation in the nucleus accumbens was observed in the natural-enriched animals. Thus, the current findings indicate the potential importance of exposure to complex environments, especially natural-like habitats, in the maintenance of emotional health, perhaps providing a buffer against the emergence of anxiogenic responses.
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Several studies have suggested that the thalamic centromedian-parafascicular (CM/PF or the PF in rodents) is implicated in the pathophysiology of Parkinson's disease (PD). However, inconsistent changes in the neuronal firing rate and pattern have been reported in parkinsonian animals. To investigate the impact of a dopaminergic cell lesion on PF extracellular discharge in behaving rats, the PF neural activities in the spike and local field potential (LFP) were recorded in unilaterally 6-hydroxydopamine- (6-OHDA) lesioned and neurologically intact control rats during rest and limb movement. ⋯ However, dopamine lesioning was associated with a decrease in neuronal spiking fire rate and reshaping in the firing pattern in the PF. The simultaneously recorded LFP activity exhibited a significant increase in power at 12-35Hz and a decrease in power at 0.7-12Hz compared with the control rats. These findings indicate that 6-OHDA induces modifications in PF spike and LFP activities in rats during rest and movement and suggest that PF dysfunction may be an important contributor to the pathophysiology of parkinsonian motor impairment.
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This study aimed to test the hypothesis that, during extended wakefulness, parasympathetic activity is associated with the depth of the subsequent recovery sleep in mice. Fourteen male C57BL/6 mice were implanted with electrodes for sleep recording. Continuous spectral analysis was performed on the electroencephalogram (EEG) to obtain theta power (6-9Hz) and delta power (0-4Hz), as well as the R-R interval signals in order to quantify the high-frequency power (HF) and normalized low-frequency power (LF%) that are used to assess parasympathetic and sympathetic activity, respectively. ⋯ Both the rise in HF and theta power during extended wakefulness were found to be positively correlated with the delta power rebound. Furthermore, the HF change during extended wakefulness was also correlated with the amount of sleep loss and the enhancement of waking theta power. Our finding suggests that waking parasympathetic activity intimately reflects the cumulative sleep pressure, suggesting a potential role to be an autonomic marker for sleep propensity.
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Decrease in brain amyloid-β (Aβ) accumulation is a leading strategy for treating Alzheimer's disease (AD). However, the intrinsic mechanism of the regulation of brain Aβ production is largely unknown. Previously, we reported that ILEI (also referred to as FAM3C) binds to the γ-secretase complex and suppresses Aβ production without inhibiting γ-secretase activity. ⋯ ILEI expression levels in brain peaked during the postnatal period and declined with age. In comparison with age-matched control brains, the number of ILEI-immunoreactive neurons decreased in AD brains, although the subcellular localization was unaltered. Our results suggest that a decline of ILEI expression may cause accumulation of Aβ in the brain and the eventual development of AD.