Neuroscience
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Comparative Study
Masking Differentially Affects Envelope-following Responses in Young and Aged Animals.
Age-related hearing decline typically includes threshold shifts as well as reduced wave I auditory brainstem response (ABR) amplitudes due to cochlear synaptopathy/neuropathy, which may compromise precise coding of suprathreshold speech envelopes. This is supported by findings with older listeners, who have difficulties in envelope and speech processing, especially in noise. However, separating the effects of threshold elevation, synaptopathy, and degradation by noise on physiological representations may be difficult. ⋯ High-pass noise may affect EFR amplitudes in young animals more than aged by reducing the contributions of high-frequency-sensitive inputs. EFRs to SAM tones in modulated noise (NAM) suggest that neurons of young animals can synchronize to NAM at lower sound levels and maintain dual AM representations better than older animals. The overall results show that EFR amplitudes are strongly influenced by aging and the presence of a competing sound that likely reduces or shifts the pool of responsive neurons.
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Human spatial manipulation ability is sensitive to high-altitude (HA) environment. The present study aimed to investigate the electrophysiological basis of spatial manipulation ability on adult immigrants with long-term HA exposure using the mental rotation (MR) task and the ERP approach. Toward this end, we explored the MR effect in individuals who immigrated to HA areas for three years compared with individuals who lived in low altitude areas. ⋯ The ERP component analysis further indicated that the rotation-related negativity (RRN) amplitude was highly corresponding to the MR effect in each group, the RRN amplitude was significantly larger in the HA group than the low-altitude group related to each rotation angle condition. The brain topographical map further showed that only the right hemisphere regions instead of the bilateral hemisphere regions involved into the MR effect in the HA group, which was different to the low-altitude group. Together, these findings might collectively suggest that the mental resource was insufficient as a result of HA exposure which can be reflected on the RRN amplitude, which may help understanding the neural basis of spatial ability change from the long-term HA exposure.
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Although the precise mechanism of action of antidepressant drugs remains elusive, the neuroplastic hypothesis has gained acceptance during the last two decades. Several studies have shown that treatment with antidepressants such as Fluoxetine is associated with enhanced plasticity in control animals, especially in regions such as the visual cortex, the hippocampus and the medial prefrontal cortex. More recently, the basolateral amygdala has been shown to be affected by Fluoxetine leading to a reopening of critical period-like plasticity in the fear and aggression circuits. ⋯ Here we show that Fluoxetine reorganizes inhibitory circuits through increased expression of the plasticity-related molecule PSA-NCAM which regulates interneuronal structure and connectivity. In addition, we demonstrate that treatment with this antidepressant alters the structure of somatostatin interneurons both at the level of dendritic spines and of axonal en passant boutons. Our findings suggest that new strategies targeting somatostatin interneuron activity might help us to better understand depression and the action of antidepressants.
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β-Amyloid (Aβ) plays an important role in the early pathogenesis of Alzheimer's disease (AD). In vitro studies have demonstrated that Aβ oligomers induce hippocampal and neocortical neuronal death. However the neurotoxic mechanisms by which soluble Aβ oligomers cause neuronal damage and death remain to be fully elucidated. ⋯ The C-terminal region of NSP3 unbound to a Cas protein was necessary for the NSP3-induced acceleration of neuronal death, as was Cas-independent Rap1A activation downstream of NSP3. Moreover, NSP3 RNAi knockdown partially rescued Aβ-oligomer-treated neurons. These results indicate that NSP3 upregulation by soluble Aβ oligomers may accelerate neuronal death via Cas-independent Rap1A activation, implicating NSP3 in the pathogenesis of AD.
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Pregnancy is accompanied by complex biological adaptations, including extreme hormonal fluctuations. Moreover, changes on the endocrine level are accompanied by changes in cerebral anatomy, such as reductions in brain or gray matter volume. Since declining brain and tissue volumes are characteristic for normal aging, the question arises of whether such pregnancy-induced anatomical effects are permanent or transient. ⋯ Comparing the BrainAGE indices between both time points, female brains at late postpartum were estimated to be considerably younger than at early postpartum. On average, that difference was about five years (mean ± SD: 5.4 ± 2.4 years). These findings suggest a substantial restoration/rejuvenation effect after giving birth, which is evident already within the first couple of months.