Subjects: Psychology >> Cognitive Psychology submitted time 2024-05-03
Abstract： While previous studies have primarily focused on exploring the sources of time perception bias at an individual level, limited research has been conducted on understanding the mechanisms behind time perception bias in social contexts. To fill this gap, the present study combined a joint action paradigm with a time perception paradigm to investigate time perception in social contexts and further examine the mechanisms of co-representation and/or social facilitation in joint temporal perception through three experiments.
In general, the study utilized a between-subject 2 x 2 experimental design, with the factors of context (individual vs. joint) and duration distribution (short intervals vs. long intervals). The stimulus durations were either 400 ms or 1000 ms for the short interval group, and 1000 ms or 1600 ms for the long interval group. The different intervals were filled with either yellow or green circles. Participants first completed a learning task alone and then were randomly assigned to either an individual or joint context and completed a practice task. In the joint condition, two participants not knowing each other practiced in different temporal intervals and completed the experiment together. In the individual condition, one participant sat alone on the left or right side of the screen and completed the experiment. During the learning phase, participants were familiarized with the short- and long-interval stimuli. During the practice phase, orange solid circles of different durations (ranging from 400 ms to 1000 ms, in steps of 100 ms) or green solid circles (ranging from 1000 ms ~ 1600 ms, in steps of 100 ms) were randomly presented on the screen. Participants judged whether the duration of the stimulus was short or long according to the criteria formed during the learning phase.
In Experiment 1, we discovered that individuals’ subjective equivalence points were significantly altered, and their sensitivity to time perception was notably reduced in joint situations compared to individual situations. In Experiment 2, we stimulated co-representation by manipulating beliefs, and the absence of peers weakened the strength of social inhibition. The results indicated that individuals exhibited similar shifts in subjective equivalence points as observed in joint situations, but there was no significant change in temporal perceptual sensitivity. In Experiment 3, the effect of co-representation was attenuated by manipulating the peer’s task goal to be a non-temporal estimation task, while the presence of peers elicited social inhibition. The findings demonstrated a significant decrease in individuals’ time-perception sensitivity compared to the individual situation, but no significant shift in subjective equivalence points.
In summary, the present study suggests that individuals in joint action contexts represent their peers’ task information through the mechanism of co-representation, which introduces bias in time estimation. Additionally, the presence of others competes for attentional resources, leading to a reduction in individuals’ sensitivity to time perception in joint action contexts.
Peer Review Status:
Awaiting Review
Subjects: Psychology >> Social Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： Multi-sensory integration (MSI), also known as multi-modal integration, refers to a comprehensive process of selecting, connecting, unifying, and interpreting different sensory information. It involves coordination among various functional brain regions to achieve temporal binding of multiple sensory information and global predictive coding. On the other hand, the gamma rhythm oscillation (i.e., γ-band oscillation, at 30-100 Hz), as a type of neural oscillatory activity with low amplitude but high frequency, widely exists in different brain areas. Gamma rhythm oscillation mainly originates from the responses of glutamic acid of the supragranular layers to external stimuli, while this response is synchronously modulated by gamma-aminobutyric acid (GABA) interneurons. Recent research has shown that gamma rhythm oscillation plays a critical role in perceptual process due to its multiple functions in reflecting excitation/inhibition balance of interneurons, implementing temporal binding of multi-sensory information, and participating in global predictive coding via a cross-frequency coupling mechanism. On the other hand, MSI deficits are typical comorbidities of autism spectrum disorders (ASD) and usually found in ASD children from 7 to 12 years of age in the growth and development period. The main clinical manifestation of MSI deficits in ASD is that the patients have difficulties in combining with multi-sensory information efficiently, and even show abnormal perception such as hyper- or hypo-sensitivity. Under laboratory conditions, the MSI deficits in ASD could be illustrated as lacking multisensory redundant target effect, wider but symmetrical temporal binding window, weaker ability of rapid audiovisual temporal recalibration, and few illusions in multi-sensory integration. From the perspective of MSI deficits in ASD, this article systematically reviews previous theories in abnormal perception of ASD, which include the minicolumn pathology hypothesis (Casanova et al., 2002), the temporal binding deficit hypothesis (Brock et al., 2002), the predictive coding deficit hypothesis (Chan et al., 2016), and the cross-frequency coupling hypothesis (Kessler et al., 2016). We also analyze the physio-psychological mechanisms of ASD’s MSI deficits in combination with their abnormal gamma rhythm oscillations. We argue that abnormal gamma rhythm oscillations should be treated as an important biomarker of MSI deficits in ASD. Specifically, compared with healthy controls, children with ASD usually exhibit abnormal gamma oscillations caused by their structural and functional abnormalities in GABA interneurons (i.e., impaired minicolumn). In turn, the abnormalities in GABA interneurons indexed by gamma oscillations would interfere the functional gamma feedforward connectivity and then disrupt the normal temporal binding and predictive encoding, and thus eventually cause MSI deficits. Although gamma rhythm oscillations in ASD have high correlations with their MSI deficits, it should be noted that the gamma rhythm oscillations might be one of the critical biomarkers of MSI deficits, but not the only one. Previous research has also shown that the alpha rhythm oscillations could also reflect the MSI deficits in ASD. In addition, interventions on abnormal gamma rhythm oscillations could improve clinical symptoms of MSI deficits in children with ASD, but may not able to fully resolve their multi-sensory integration problems. Therefore, as a biomarker of MSI deficits in ASD, gamma rhythm oscillations should to be used in caution. Nevertheless, given a causal link existed between gamma neural oscillations and MSI deficits in ASD, future research could use gamma rhythm neural oscillation as a biofeedback indicator, in combination with non-invasive and reversible intervention technologies (e.g., repetitive Transcranial Magnetic Stimulation, rTMS), to develop scientific and systematic clinical interventions.
Subjects: Psychology >> Physiological Psychology Subjects: Psychology >> Applied Psychology submitted time 2020-08-07
Abstract： Multi-sensory integration (MSI) refers to a comprehensive process of selecting, connecting, unifying, and interpreting different sensory information. It involves coordination among various brain regions to achieve temporal binding of multiple sensory information and global predictive encoding. On the other hand, gamma oscillation plays vital roles in MSI, due to its versatile functions in reflecting excitation/inhibition balance of interneuron, implementing temporal binding of multi-sensory information, and participating in global predictive encoding via a cross-frequency coupling mechanism. Multisensory integration deficits are typical symptoms of patients with autism spectrum disorders (ASD). Research shows that patients with ASD usually exhibit abnormal gamma oscillations caused by structural and functional abnormalities in GABA interneurons. In turn, these abnormal gamma oscillations disrupt temporal binding and predictive encoding, and eventually lead to MSI deficits in ASD. As a result, future research could use gamma rhythm neural oscillation as a biofeedback indicator, in combination with non-invasive and reversible intervention technologies, to develop scientific and systematic clinical intervention treatments. " " "
Peer Review Status:Awaiting Review
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