Neuroscience
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Synapse or dendritic spine loss is the strongest correlate of cognitive decline in Alzheimer's disease (AD), and neurofibrillary tangles (NFTs), but not amyloid-β plaques, associate more closely with transition to mild cognitive impairment. Yet, how dendritic spine architecture is affected by hyperphosphorylated tau is still an ongoing question. To address this, we combined cell and biochemical analyses of the Tau P301S mouse line (PS19). ⋯ This suggests that CA1 pyramidal neurons in PS19 mice may undergo spine remodeling in response to tau accumulation and age. In the mPFC, spine density was similar among PS19 mice and NTG littermates at 6 and 9 months, but age-related reductions in synaptic tau levels were observed among PS19 mice. Collectively, these studies reveal brain region-specific changes in dendritic spine density and morphology in response to age and the presence of hyperphosphorylated tau in the PS19 mouse line.
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The process of learning and playing a musical instrument modulates the structural and functional organization of cortical motor networks. In the present study the excitability and short-term functional plasticity of face and hand areas of primary motor cortex (M1) were compared in woodwind musicians (WM), string musicians (SM) and non-musicians (NM) to test the hypothesis that neurophysiological adaptations to the long-term experience of playing a musical instrument are site-specific and related to the particular physiological properties of the representation area in M1. Twenty-two musicians (11 SM, 11 WM) and 11 NM participated in the study. ⋯ WM exhibited significant IHI in the DAO (p = 0.031), in contrast to its absence in SM and NM. Compared with NM and WM, the PAS-induced increase in MEP amplitude in SM was significantly larger in hand M1 (p = 0.008) but not in face M1. In conclusion, neurophysiological adaptations differ between WM, in whom control of the embouchure is highly important, and SM who perform a large range of sequential finger movements and are site-specific in M1.
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Excessive exposure to loud noise causes hearing loss and neural plasticity throughout the auditory pathway. Recent studies have identified that non-auditory regions, such as the hippocampus, are also susceptible to noise exposure; however, the electrophysiological and behavioral consequences of noise-induced hearing loss on the prefrontal cortex (PFC) are unclear. Using chronically-implanted electrodes in awake rats, we investigated neural plasticity in the auditory and prefrontal cortices in the days following noise exposure via metrics associated with spontaneous neural oscillations and the 40-Hz auditory steady-state response (ASSR). ⋯ Moreover, phase synchrony between auditory and prefrontal cortices was decreased post-exposure, suggesting a reduction in functional connectivity. Cognitive-behavioral testing using the Morris water maze and a series of lever-pressing tasks revealed that noise exposure impaired spatial learning and reference memory, as well as stimulus-response habit learning, whereas cognitive flexibility tasks requiring set-shifting and reversal learning appeared unaffected. Collectively, our findings identify the complex and region-specific cortical plasticity associated with noise-induced hearing loss, and highlight the varying degrees of susceptibility of non-auditory, cognitive tasks of learning, memory and executive function to noise exposure.
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Clearance of dysfunctional mitochondria via mitophagy is essential for cell survival and cochlear functions. However, it is not clear which genes are significantly involved in this process. Here, we investigated the changes in mitophagy and mitophagy-associated genes in mouse auditory cells to determine a possible correlation between mitophagy and age-related hearing loss (ARHL). ⋯ Mitophagy-inhibited cells with BNIP3L/NIX knockdown showed hyperresponsiveness to oxidative stress resulting in cell senescence with increased levels of TOMM20 and LC3B. Overexpression of BNIP3L/NIX promotes the degradation of TOMM20 and LC3B during premature cell senescence. In conclusion, BNIP3L/NIX may play an important role in mitochondria degradation maintaining cochlear cell homeostasis during the aging process of hearing.
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The val66met polymorphism of the brain-derived neurotrophic factor gene has been associated with changes in components of executive functioning such as decision making; however, this relationship remains unclear. Val66met-related changes in attention and visual processing speed may explain potential changes in decision making. Furthermore, chronic stress disrupts executive functions and alters autonomic activity. ⋯ Neither stress nor autonomic activity moderated the effect of val66met on decision making or attention. This study is the first to investigate the role of val66met in decision making, attention, and visual processing while taking into account chronic stress and autonomic activity. This multifactorial approach revealed that carriers of the Val/met genotype may have better decision making and attention than Val/val carriers.