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| http://dx.doi.org/10.1038/s41386-022-01382-6 | DOI Listing |
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Ondansetron blocks fluoxetine effects in immature neurons in the adult rat piriform cortex layer II.
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Neurobiology Unit, Institute for Biotechnology and Biomedicine (BIOTECMED), University of Valencia, Spain. Electronic address:
Neuronal structural plasticity gives the adult brain the capacity to adapt to internal or external factors by structural and molecular changes. These plastic processes seem to be mediated, among others, by the action of the neurotransmitter serotonin through specific receptors (5-HTRs). Previous studies have shown that the maturation of granule cells in the hippocampus is mediated by 5-HT3.
View Article and Find Full Text PDFThe Impact of Sleep and Exercise on Brain Atrophy in Mild Cognitive Impairment.
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Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, 79430, TX, USA; Nutritional Sciences Department, College Human Sciences, Texas Tech University, Lubbock, TX 79409; Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Public Health, Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Speech, Language, and Hearing Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. Electronic address:
Chronic sleep deprivation and lack of physical exercise may have detrimental effects on overall health, particularly in terms of brain health, with significant implications for cognitive function and well-being. This review explores the impact of chronic sleep deprivation and physical exercise on brain atrophy in mild cognitive impairment (MCI) and Alzheimer's disease (AD). Drawing insights from 40 selected studies, the review synthesizes evidence on these lifestyle factors' correlations with neurodegenerative changes.
View Article and Find Full Text PDFFamilial Alzheimer's disease mutations in amyloid precursor protein impair calcineurin signaling to NMDA receptors.
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Department of Pharmacology, Addiction Science, and Toxicology, College of Medicine, The University of Tennessee Health Science Center; Memphis, 38163. Electronic address:
Familial Alzheimer's disease (FAD) is frequently associated with mutations in the amyloid precursor protein (APP), which are thought to lead to cognitive deficits by impairing NMDA receptor (NMDAR)-dependent forms of synaptic plasticity. Given the reliance of synaptic plasticity on NMDAR-mediated Ca entry, shaping of NMDAR activity by APP and/or its disease-causing variants could provide a basis for understanding synaptic plasticity impairments associated with FAD. A region of APP (residues 639-644 within APP695) processed by the γ-secretase complex, which generates amyloid β (Aβ) peptides, is a hotspot for FAD mutations.
View Article and Find Full Text PDFDye Molecule-Induced Optoelectronic Synaptic Behaviors of Monolayer MoSe.
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School of Mathematics and Physics, University of Science and Technology Beijing, Beijing 100083, China.
Although MoSe-based photodetectors have achieved excellent performance, the ultrafast photoresponse has limited their application as an optoelectronic synapse. In this paper, the enhancement of the rhodamine 6G molecule on the memory time of MoSe is reported. It is found that the memory time of monolayer MoSe can be obviously enhanced after assembly with rhodamine 6G exhibiting synaptic characteristics in comparison to pristine MoSe.
View Article and Find Full Text PDFSpinally targeted paired associated stimulation with high-frequency peripheral component induces spinal level plasticity in healthy subjects.
Sci Rep
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BioMag Laboratory, HUS Diagnostic Center, Helsinki University Hospital, University of Helsinki and Aalto University School of Science, Helsinki, Finland.
A novel variant of paired-associative stimulation (PAS) consisting of high-frequency peripheral nerve stimulation (PNS) and high-intensity transcranial magnetic stimulation (TMS) above the motor cortex, called high-PAS, can lead to improved motor function in patients with incomplete spinal cord injury. In PAS, the interstimulus interval (ISI) between the PNS and TMS pulses plays a significant role in the location of the intended effect of the induced plastic changes. While conventional PAS protocols (single TMS pulse often applied with intensity close to resting motor threshold, and single PNS pulse) usually require precisely defined ISIs, high-PAS can induce plasticity at a wide range of ISIs and also in spite of small ISI errors, which is helpful in clinical settings where precise ISI determination can be challenging.
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