Neuroscience
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Reconsolidation results in the restabilisation, and thus persistence, of a memory made labile by retrieval, and interfering with this process is thought to enable modification or weakening of the original trace. As such, reconsolidation-blockade has been a focus of research aiming to target the maladaptive memories underlying mental health disorders, including post-traumatic stress disorder and drug addiction. Current first-line therapies are not effective for all patients, and a substantial proportion of those for whom therapies are effective later relapse. ⋯ These include factors such as the age and strength of memory, and can broadly be divided into two categories: intrinsic features of the targeted memory itself, and parameters of the reactivation procedure used. With maladaptive memory characteristics inevitably varying amongst individuals, manipulation of the other limitations imposed by procedural variables have been explored to circumvent the boundary conditions on reconsolidation. Although several apparently discrepant results remain to be reconciled and these limitations yet to be truly defined, many studies have produced successful results which encouragingly demonstrate that boundary conditions may be overcome using various proposed strategies to enable translation of a reconsolidation-based intervention to clinical use.
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Predictions of incoming words performed during reading have an impact on how the reader moves their eyes and on the electrical brain potentials. Eye tracking (ET) experiments show that less predictable words are fixated for longer periods of times. Electroencephalography (EEG) experiments show that these words elicit a more negative potential around 400 ms (N400) after the word onset when reading one word at a time (foveated reading). ⋯ Our results show that the N400 potential disappear when the reader recognises the sentence. Furthermore, time-frequency analyses show a larger alpha lateralisation and a beta power increase for memory-encoded sentences. This suggests a more distributed attention and an active maintenance of the cognitive set, in concordance to the predictive coding framework.
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The effects of traditional treatments for peripheral nerve injury (PNI) are not ideal, which has prompted the identification of new therapeutic strategies. As unique glial cells in the peripheral nervous system, Schwann cells (SCs) play an important role in the repair of PNI. Recent studies have demonstrated that long noncoding RNAs (lncRNAs) are involved in the regulation of nerve repair after PNI. ⋯ Expression of lncRNA Sox2ot was increased after PNI, and overexpression of Sox2ot promoted SCs migration and proliferation. Mechanistic analyses confirmed that Sox2ot can regulate the expression of Cthrc1 through competitive adsorption of miR-9 in SCs, ultimately affecting SCs migration and proliferation. Our findings reveal the key role of lncRNA Sox2ot in nerve regeneration and provide a new direction for PNI treatment.
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According to the correlated transmitter-receptor based structure of the inferior parietal cortex (IPC), this brain area is divided into three clusters, namely, the caudal, the middle and the rostral. Nevertheless, in associating different cognitive functions to the IPC, previous studies considered this part of the cortex as a whole and thus inconsistent results have been reported. Using multiband echo planar imaging (EPI), we investigated the connectivity profile of the middle IPC while forty-five participants performed a task requiring cognitive control. ⋯ At the same time, this cortical area showed negative functional connectivity with both the precuneus cortex, which is resting- state related, and brain areas related to general cognitive functions. That is, the functions of the middle IPC are not accommodated by the traditional categorization of different brain areas i.e. resting state-related or task-related networks and this advanced our hypothesis about modulating cortical areas. Such brain areas are characterized by their negative functional connectivity with parts of the cortex involved in task performance, proportional to the difficulty of the task; yet, their functional associations are inconsistent with the resting state-related cortical areas.
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The circadian clock can coordinate, regulate and predict physiology and behavior in response to the standard light-dark (LD: 12 h light and 12 h dark) cycle. If we alter the LD cycle by exposing mice to constant darkness (DD: 00 h light and 24 h dark), it can perturb behavior, the brain, and associated physiological parameters. The length of DD exposure and the sex of experimental animals are crucial variables that could alter the impact of DD on the brain, behavior, and physiology, which have not yet been explored. ⋯ Three weeks of restoration was adequate to establish homeostasis in both sexes. To the best of our knowledge, this study is the first of its kind to look at how DD exposure impacts physiology and behavior as a function of sex- and time. These findings would have translational value and may help in establishing sex-specific interventions for addressing DD-related psychological issues.