Neuroscience
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Editorial Comment
Distinguishing between synaptic vesicles in different functional states.
Editorial on Non-negative matrix factorization as a tool to distinguish between synaptic vesicles in different functional states.
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Accumulation of amyloid peptides in the brain plays a key role in the pathogenesis of Alzheimer's disease (AD). Aggregated beta-amyloid (Aβ) peptide increases intracellular reactive oxygen species associated to a deficient antioxidant defense system. Prefrontal cortex plays a key role in memory and learning and is especially susceptible to oxidative stress. ⋯ Interestingly, we found that an i.c.v. injection of Aβ(1-42) increased lipid peroxidation, reduced total antioxidant capacity level, phase-shifted the daily peak of reduced glutathione, and had a differential effect on the oscillating catalase and glutathione peroxidase specific activity. Thus, elevated levels of Aβ aggregates-a pathogenic hallmark of AD, caused altered temporal patterns of the cellular redox state in prefrontal cortex rat. These findings might contribute, at least in part, to the understanding of the molecular and biochemical basis of redox changes caused by circadian rhythms alterations observed in AD patients.
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Increasing evidence has indicated that long non-coding RNAs (lncRNAs) play a vital role for adjusting RNA transcripts as competing endogenous RNAs (ceRNAs) for microRNAs (miRNAs). The present study was intended to explore the probable regulation of lncRNA TALNEC2 in ischemic stroke. In this study, we measured the up-regulation of TALNEC2 and down-regulation of miR-650 in mice brains after cerebral ischemia/reperfusion (I/R) operation and in cultured neuroblastoma cells of neuro-2A (N2a) treated with oxygen glucose deprivation/reoxygenation (OGD/R). ⋯ In result, overexpression of TALNEC2 antagonized the inhibition impact of miR-650 on APAF1 expression and N2a cell apoptosis induced by OGD/R, while TALNEC2 knockdown aggravated the impact. Furthermore, TALNEC2 knockdown reversed brain injury and neurological deficits induced by I/R in vivo. In conclusion, we verified a TALNEC2/miR-650/APAF1 signaling pathway as a key mechanism monitoring cerebral I/R injury.
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Differences in the intrinsic properties of intralaminar thalamo-striatal neurons such as expressing low-threshold-spikes (LTS) or after hyperpolarizing potentials (AHPs) of different duration have been attributed to different maturation stages. However, two morphological types: "diffuse" and "bushy" have been described. Therefore, we explored whether electrophysiological differences persist in adult mice using whole cell recordings. ⋯ Both cell classes could fire in two modes: trains of single action potentials at depolarized potentials or high frequency bursts on top of LTS at more hyperpolarized potentials. LTS were probably generated by Cav3 calcium channels since they were blocked by the selective antagonist TTA-P2. About 11% of neurons with brief AHPs and 55% of neurons with prolonged AHPs do not show LTS and bursts, even when potassium currents are blocked.
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Sensory substitution refers to the concept of feeding information to the brain via an atypical sensory pathway. We here examined the degree to which participants (deaf and hard of hearing) can learn to identify sounds that are algorithmically translated into spatiotemporal patterns of vibration on the skin of the wrist. In a three-alternative forced choice task, participants could determine the identity of up to 95% and on average 70% of the stimuli simply by the spatial pattern of vibrations on the skin. ⋯ Participants answered whether the word was the same or different. With minimal difference pairs (distinguished by only one phoneme, such as "house" and "mouse"), the best performance was 83% (average of 62%), while with non-minimal pairs (such as "house" and "zip") the best performance was 100% (average of 70%). Collectively, these results demonstrate that participants are capable of using the channel of the skin to interpret auditory stimuli, opening the way for low-cost, wearable sensory substitution for the deaf and hard of hearing communities.