scholarly journals Is Sleep Essential for Neural Plasticity in Humans, and How Does It Affect Motor and Cognitive Recovery?

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Maurizio Gorgoni ◽  
Aurora D'Atri ◽  
Giulia Lauri ◽  
Paolo Maria Rossini ◽  
Fabio Ferlazzo ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Sleep Quality ◽  
Beneficial Effect ◽  
Neural Plasticity ◽  
Point Of View ◽  
Specific Nature ◽  
Synaptic Homeostasis ◽  
Recovery Processes ◽  
Cortical Topography ◽  
Underlying Mechanisms

There is a general consensus that sleep is strictly linked to memory, learning, and, in general, to the mechanisms of neural plasticity, and that this link may directly affect recovery processes. In fact, a coherent pattern of empirical findings points to beneficial effect of sleep on learning and plastic processes, and changes in synaptic plasticity during wakefulness induce coherent modifications in EEG slow wave cortical topography during subsequent sleep. However, the specific nature of the relation between sleep and synaptic plasticity is not clear yet. We reported findings in line with two models conflicting with respect to the underlying mechanisms, that is, the “synaptic homeostasis hypothesis” and the “consolidation” hypothesis, and some recent results that may reconcile them. Independently from the specific mechanisms involved, sleep loss is associated with detrimental effects on plastic processes at a molecular and electrophysiological level. Finally, we reviewed growing evidence supporting the notion that plasticity-dependent recovery could be improved managing sleep quality, while monitoring EEG during sleep may help to explain how specific rehabilitative paradigms work. We conclude that a better understanding of the sleep-plasticity link could be crucial from a rehabilitative point of view.

scholarly journals The Maternal Brain: An Organ with Peripartal Plasticity

2014 ◽  
Vol 2014 ◽  
pp. 1-20 ◽  
Author(s):  
Katharina Maria Hillerer ◽  
Volker Rudolf Jacobs ◽  
Thorsten Fischer ◽  
Ludwig Aigner
Keyword(s):  
Mental Health ◽  
Synaptic Plasticity ◽  
Neural Plasticity ◽  
Molecular Mechanisms ◽  
Brain Regions ◽  
Tight Control ◽  
Maternal Brain ◽  
Pregnancy And Lactation ◽  
Underlying Mechanisms ◽  
And Behavior

The time of pregnancy, birth, and lactation, is characterized by numerous specific alterations in several systems of the maternal body. Peripartum-associated changes in physiology and behavior, as well as their underlying molecular mechanisms, have been the focus of research since decades, but are still far from being entirely understood. Also, there is growing evidence that pregnancy and lactation are associated with a variety of alterations in neural plasticity, including adult neurogenesis, functional and structural synaptic plasticity, and dendritic remodeling in different brain regions. All of the mentioned changes are not only believed to be a prerequisite for the proper fetal and neonatal development, but moreover to be crucial for the physiological and mental health of the mother. The underlying mechanisms apparently need to be under tight control, since in cases of dysregulation, a certain percentage of women develop disorders like preeclampsia or postpartum mood and anxiety disorders during the course of pregnancy and lactation. This review describes common peripartum adaptations in physiology and behavior. Moreover, it concentrates on different forms of peripartum-associated plasticity including changes in neurogenesis and their possible underlying molecular mechanisms. Finally, consequences of malfunction in those systems are discussed.

scholarly journals Erasing Synapses in Sleep: Is It Time to Be SHY?

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Marcos Gabriel Frank
Keyword(s):  
Drosophila Melanogaster ◽  
Synaptic Plasticity ◽  
Functional Significance ◽  
Brain Plasticity ◽  
Cellular Mechanism ◽  
Homeostatic Regulation ◽  
Synaptic Homeostasis ◽  
Underlying Mechanisms ◽  
The Brain ◽  
Lines Of Evidence

Converging lines of evidence strongly support a role for sleep in brain plasticity. An elegant idea that may explain how sleep accomplishes this role is the “synaptic homeostasis hypothesis (SHY).” According to SHY, sleep promotes net synaptic weakening which offsets net synaptic strengthening that occurs during wakefulness. SHY is intuitively appealing because it relates the homeostatic regulation of sleep to an important function (synaptic plasticity). SHY has also received important experimental support from recent studies inDrosophila melanogaster. There remain, however, a number of unanswered questions about SHY. What is the cellular mechanism governing SHY? How does it fit with what we know about plasticity mechanisms in the brain? In this review, I discuss the evidence and theory of SHY in the context of what is known about Hebbian and non-Hebbian synaptic plasticity. I conclude that while SHY remains an elegant idea, the underlying mechanisms are mysterious and its functional significance unknown.

scholarly journals Intranasal insulin rescues repeated anesthesia-induced deficits in synaptic plasticity and memory and prevents apoptosis in neonatal mice via mTORC1

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Patricia Soriano Roque ◽  
Mehdi Hooshmandi ◽  
Laura Neagu-Lund ◽  
Shelly Yin ◽  
Noosha Yousefpour ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
General Anesthesia ◽  
Preventive Treatment ◽  
Intranasal Insulin ◽  
Translational Repressor ◽  
Beneficial Effects ◽  
Underlying Mechanisms ◽  
Induced Apoptosis ◽  
Preclinical And Clinical Studies

AbstractLong-lasting cognitive impairment in juveniles undergoing repeated general anesthesia has been observed in numerous preclinical and clinical studies, yet, the underlying mechanisms remain unknown and no preventive treatment is available. We found that daily intranasal insulin administration to juvenile mice for 7 days prior to repeated isoflurane anesthesia rescues deficits in hippocampus-dependent memory and synaptic plasticity in adulthood. Moreover, intranasal insulin prevented anesthesia-induced apoptosis of hippocampal cells, which is thought to underlie cognitive impairment. Inhibition of the mechanistic target of rapamycin complex 1 (mTORC1), a major intracellular effector of insulin receptor, blocked the beneficial effects of intranasal insulin on anesthesia-induced apoptosis. Consistent with this finding, mice lacking mTORC1 downstream translational repressor 4E-BP2 showed no induction of repeated anesthesia-induced apoptosis. Our study demonstrates that intranasal insulin prevents general anesthesia-induced apoptosis of hippocampal cells, and deficits in synaptic plasticity and memory, and suggests that the rescue effect is mediated via mTORC1/4E-BP2 signaling.

scholarly journals Exposure to relaxing words during sleep promotes slow-wave sleep and subjective sleep quality

2020 ◽  
Author(s):  
Jonas Beck ◽  
Erna Loretz ◽  
Björn Rasch
Keyword(s):  
Sleep Quality ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Well Being ◽  
Subjective Sleep Quality ◽  
Sleep Depth ◽  
Activity Band ◽  
Underlying Mechanisms ◽  
Healthy Participants ◽  
Subjective Level

AbstractOur thoughts alter our sleep, but the underlying mechanisms are still unknown. We propose that mental processes are active to a greater or lesser extent during sleep and that this degree of activation affects our sleep depth. We examined this notion by activating the concept of “relaxation” during sleep using relaxation-related words in 50 healthy participants. In support of our hypothesis, playing relaxing words during non-rapid eye movement sleep extended the time spent in slow-wave sleep, increased power in the slow-wave activity band after the word cue, and abolished an asymmetrical sleep depth during the word presentation period. On the subjective level, participants reported a higher sleep quality and elevated alertness ratings. Our results support the notion that the activation of mental concepts during sleep can influence sleep depth and provide a basis for interventions using targeted activations to promote sleep depth and sleep quality to foster well-being and health.

PRIMARY PREVENTION OF DEMENTIA: AN EPIDEMIOLOGICAL POINT OF VIEW

2016 ◽  
pp. 1-4
Author(s):  
C. Berr
Keyword(s):  
Risk Factors ◽  
Primary Prevention ◽  
Disease Onset ◽  
Point Of View ◽  
Level Of Evidence ◽  
Life Course Approach ◽  
Important Concern ◽  
Dementia Prevention ◽  
Underlying Mechanisms ◽  
The Impact

From an epidemiological perspective, in order to increase the level of evidence, it is necessary to refer to data from longitudinal studies to validate the temporal relationship between exposure (e.g. the behavior or modifying factor) and the disease. Findings from such studies are useful for defining risk factors and laying the groundwork for proposing interventions for prevention. This step is crucial in order to define the periods (life-course approach) and groups at risk, which will then become the targets of interventions designed to modify behaviors or lifestyle. Specifying the underlying mechanisms of these risk factors is one of the objectives of etiological epidemiology which focuses on the origin of diseases but is not essential for a more pragmatic interventional approach. These questions are essential for dementia prevention and are discussed in this paper. Furthermore, timing interventions is a major problem even if we identify primary prevention pathways in dementia. Another important concern for epidemiologists is the need to make projections to estimate the number of dementia cases in the next decades considering different intervention scenarios. These models require adequate descriptive indicators of dementia, demography and mortality and precise estimations of the impact of potential interventions in terms of delaying disease onset for instance.

scholarly journals Noise Induced Hearing Loss and Tinnitus—New Research Developments and Remaining Gaps in Disease Assessment, Treatment, and Prevention

2020 ◽  
Vol 10 (10) ◽  
pp. 732
Author(s):  
Tang-Chuan Wang ◽  
Ta-Yuan Chang ◽  
Richard Tyler ◽  
Ying-Ju Lin ◽  
Wen-Miin Liang ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Neural Plasticity ◽  
Noise Exposure ◽  
Disease Assessment ◽  
Noise Induced Hearing Loss ◽  
Ongoing Research ◽  
Adaptive Changes ◽  
Treatment And Prevention ◽  
Underlying Mechanisms ◽  
New Research

Long-term noise exposure often results in noise induced hearing loss (NIHL). Tinnitus, the generation of phantom sounds, can also result from noise exposure, although understanding of its underlying mechanisms are limited. Recent studies, however, are shedding light on the neural processes involved in NIHL and tinnitus, leading to potential new and innovative treatments. This review focuses on the assessment of NIHL, available treatments, and development of new pharmacologic and non-pharmacologic treatments based on recent studies of central auditory plasticity and adaptive changes in hearing. We discuss the mechanisms and maladaptive plasticity of NIHL, neuronal aspects of tinnitus triggers, and mechanisms such as tinnitus-associated neural changes at the cochlear nucleus underlying the generation of tinnitus after noise-induced deafferentation. We include observations from recent studies, including our own studies on associated risks and emerging treatments for tinnitus. Increasing knowledge of neural plasticity and adaptive changes in the central auditory system suggest that NIHL is preventable and transient abnormalities may be reversable, although ongoing research in assessment and early detection of hearing difficulties is still urgently needed. Since no treatment can yet reverse noise-related damage completely, preventative strategies and increased awareness of hearing health are essential.

scholarly journals Impairment of cerebellar long-term depression and GABAergic transmission in prion protein deficient mice ectopically expressing PrPLP/Dpl

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yasushi Kishimoto ◽  
Moritoshi Hirono ◽  
Ryuichiro Atarashi ◽  
Suehiro Sakaguchi ◽  
Tohru Yoshioka ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Prion Protein ◽  
Neural Plasticity ◽  
Late Onset ◽  
Eyeblink Conditioning ◽  
Electrophysiological Study ◽  
Synaptic Function ◽  
Long Term Depression ◽  
Underlying Mechanisms

Abstract Prion protein (PrPC) knockout mice, named as the “Ngsk” strain (Ngsk Prnp0/0 mice), show late-onset cerebellar Purkinje cell (PC) degeneration because of ectopic overexpression of PrPC-like protein (PrPLP/Dpl). Our previous study indicated that the mutant mice also exhibited alterations in cerebellum-dependent delay eyeblink conditioning, even at a young age (16 weeks of age) when neurological changes had not occurred. Thus, this electrophysiological study was designed to examine the synaptic function of the cerebellar cortex in juvenile Ngsk Prnp0/0 mice. We showed that Ngsk Prnp0/0 mice exhibited normal paired-pulse facilitation but impaired long-term depression of excitatory synaptic transmission at synapses between parallel fibres and PCs. GABAA-mediated inhibitory postsynaptic currents recorded from PCs were also weakened in Ngsk Prnp0/0 mice. Furthermore, we confirmed that Ngsk Prnp0/0 mice (7–8-week-old) exhibited abnormalities in delay eyeblink conditioning. Our findings suggest that these alterations in both excitatory and inhibitory synaptic transmission to PCs caused deficits in delay eyeblink conditioning of Ngsk Prnp0/0 mice. Therefore, the Ngsk Prnp0/0 mouse model can contribute to study underlying mechanisms for impairments of synaptic transmission and neural plasticity, and cognitive deficits in the central nervous system.

scholarly journals Civil responsability in beachwear: creation and branding / A responsabilidade civil na moda praia: criação e marca

2018 ◽  
Vol 1 (1) ◽  
pp. 24
Author(s):  
Patricia Ribeiro Serra Vieira ◽  
Anna Carolina Cazarin Queiroz
Keyword(s):  
Intellectual Property ◽  
Point Of View ◽  
Scale Production ◽  
Specific Nature ◽  
High Scale ◽  
Fast Fashion ◽  
Civil Responsibility ◽  
The Law

With the popularization of prêt-à-porter, the fashion sector and the Law have experienced an unprecedentedlevel of proximity. The rise of fast fashion stores, whose outstanding features are high-scale production andlow prices, and the increasing competition in the sector have accentuated the need to protect the industrialand intellectual property of brands and creations. In Brazil, the exuberance of its shores has resulted in thedevelopment of beachwear, a segment that we are a worldwide reference and in which there is a landmarkcourt decision with regard to the applicability of copyright in fashion creations and compensation for damagesresulting from these activities. From a casuistic and doctrinal analysis, this academic article aims to contributeto the debates on the fashion world from the point of view of civil responsibility theory, highlighting the legalsolutions applicable to the segment and the need to take into account the specific nature of this consumermarket. 

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