To further develop three-dimensional (3D) applications, it is important to elucidate the negative effects of 3D applications on the human body and mind. Thus, this study investigated differences in the effects of visual fatigue on cognition and brain activity using visual and auditory tasks induced by watching a 1-h movie in two dimensions (2D) and 3D. Eighteen young men participated in this study. Two conditions were randomly performed for each participant on different days, namely, watching the 1-h movie on television in 2D (control condition) and 3D (3D condition). Before and after watching the 1-h movie on television, critical flicker fusion frequency (CFF: an index of visual fatigue), and response accuracy and reaction time for the cognitive tasks were determined. Brain activity during the cognitive tasks was evaluated using a multi-channel near-infrared spectroscopy system. In contrast to the control condition, the decreased CFF, and the lengthened reaction time and the decreased activity around the right primary somatosensory cortex during Go/NoGo blocks in the visual task at post-viewing in the 3D condition were significant, with significant repeated measures correlations among them. Meanwhile, in the auditory task, the changes in cognitive performance and brain activity during the Go/NoGo blocks were not significant in the 3D condition. These results suggest that the failure or delay in the transmission of visual information to the primary somatosensory cortex due to visual fatigue induced by watching a 3D movie reduced the brain activity around the primary somatosensory cortex, resulting in poor cognitive performance for the visual task. This suggests that performing tasks that require visual information, such as running in the dark or driving a car, immediately after using a 3D application, may create unexpected risks in our lives. Thus, the findings of this study will help outlining precautions for the use of 3D applications.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9626648 | PMC |
| http://dx.doi.org/10.3389/fnhum.2022.974406 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Intranasal Administrations of AP39-Loaded Liposomes Selectively Deliver H2S to Neuronal Mitochondria to Protect Neonatal Hypoxia-Ischemia by Targeting ERK1/2 and Caspase-1.
ACS Biomater Sci Eng
January 2025
Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China.
Mitochondrial dysfunction contributes to the pathology of hypoxia-ischemia (HI) brain damage by aberrant production of ROS. Hydrogen sulfide (HS) has been demonstrated to exert neuroprotective effects through antioxidant mechanisms. However, the diffusion of HS is not specifically targeted and may even be systemically toxic.
View Article and Find Full Text PDFVisual activity enhances neuronal excitability in thalamic relay neurons.
Sci Adv
January 2025
Aix-Marseille Université, INSERM, UNIS, Marseille, France.
Amblyopia, a highly prevalent loss of visual acuity, is classically thought to result from cortical plasticity. The dorsal lateral geniculate nucleus (dLGN) has long been held to act as a passive relay for visual information, but recent findings suggest a largely underestimated functional plasticity in the dLGN. However, the cellular mechanisms supporting this plasticity have not yet been explored.
View Article and Find Full Text PDFDistributed representations of temporally accumulated reward prediction errors in the mouse cortex.
Sci Adv
January 2025
Lee Kong Chian School of Medicine, Nanyang Technological University, 11 Mandalay Road, Singapore 308232, Singapore.
Reward prediction errors (RPEs) quantify the difference between expected and actual rewards, serving to refine future actions. Although reinforcement learning (RL) provides ample theoretical evidence suggesting that the long-term accumulation of these error signals improves learning efficiency, it remains unclear whether the brain uses similar mechanisms. To explore this, we constructed RL-based theoretical models and used multiregional two-photon calcium imaging in the mouse dorsal cortex.
View Article and Find Full Text PDFNoncanonical role of Golgi-associated macrophage TAZ in chronic inflammation and tumorigenesis.
Sci Adv
January 2025
Department of Biochemistry, College of Life Science and Biotechnology, Brain Korea 21 Project, Yonsei University, Seoul 03722, Republic of Korea.
Until now, Hippo pathway-mediated nucleocytoplasmic translocation has been considered the primary mechanism by which yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) transcriptional coactivators regulate cell proliferation and differentiation via transcriptional enhanced associate domain (TEAD)-mediated target gene expression. In this study, however, we found that TAZ, but not YAP, is associated with the Golgi apparatus in macrophages activated via Toll-like receptor ligands during the resolution phase of inflammation. Golgi-associated TAZ enhanced vesicle trafficking and secretion of proinflammatory cytokines in M1 macrophage independent of the Hippo pathway.
View Article and Find Full Text PDFHumans excel at applying learned behavior to unlearned situations. A crucial component of this generalization behavior is our ability to compose/decompose a whole into reusable parts, an attribute known as compositionality. One of the fundamental questions in robotics concerns this characteristic: How can linguistic compositionality be developed concomitantly with sensorimotor skills through associative learning, particularly when individuals only learn partial linguistic compositions and their corresponding sensorimotor patterns? To address this question, we propose a brain-inspired neural network model that integrates vision, proprioception, and language into a framework of predictive coding and active inference on the basis of the free-energy principle.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!