Neuroscience
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Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder. Early diagnosis in the critical period is important for ASD children. Recent studies of neurodevelopmental behavioral features and joint attention in high-risk infants showed there are some special cues which can distinguish ASD from typical development infant. ⋯ Regression model showed that high fine motor scale and social behaviour scale quotient in infancy were associated with an decreased risk of the total score of CHAT-23 ≥ 2 in toddlerhood. The Receiver operating characteristic curve showed the social behaviour in infancy alone and the combination of fine motor and social behaviour in infancy contributed to auxiliary diagnosis of higher level of autistic traits in toddlerhood. These findings suggest that Impaired development of fine motor and social behavior in infancy are potential warning features of high autistic traits in general population.
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Maintenance of proper electrophysiological and connectivity profiles in the adult brain may be a perturbation point in neurodevelopmental disorders (NDDs). How these profiles are maintained within mature circuits is unclear. We recently demonstrated that postnatal ablation of the Aristaless (Arx) homeobox gene in parvalbumin interneurons (PVIs) alone led to dysregulation of their transcriptome and alterations in their functional as well as network properties in the hippocampal cornu Ammoni first region (CA1). ⋯ Current clamp recordings showed increase excitability in several sub- and threshold membrane properties that correlated with an increase in voltage-gated Na+ current. Our data suggest that, in addition to cell-autonomous disruption in PVIs, loss of Arx postnatal transcriptional activity in PVIs led to complex dysfunctions in PCs in CA1 microcircuits. These non-cell autonomous effects are likely the product of breakdown in feedback and/or feedforward processes and should be considered as fundamental contributors to the circuit mechanisms of NDDs such as Arx-linked early-onset epileptic encephalopathies.
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Schizophrenia (SCZ) is a highly heterogeneous, severe neuropsychiatric disorder of unknown etiopathology. Increasing data indicate an overlap between schizophrenia and pathological processes related to immunological dysregulation as well as inflammation, such as high levels of pro-inflammatory substances in patients' blood and cerebrospinal fluid and autoantibodies against synaptic and nerve cell membrane proteins. Autoantibodies against SFT2D2 have been reported in patients with SCZ. ⋯ Quantitative reverse transcription-polymerase chain reactions showed that the expression of pro-inflammatory genes was upregulated in the primary somatosensory cortex and hippocampus of the anti-SFT2D2-IgG-infused mice. Additionally, the mice exhibited defective sensorimotor gating, memory deficits, motor impairment, and anxiety-related behaviors without signs of depression. These findings indicate that anti-SFT2D2 autoantibodies can induce encephalitis, cause a series of behavioral changes associated with schizophrenia, and offer a model for testing novel therapies to improve treatment strategies for a subgroup of patients with SCZ.
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In conscious states, the electrodynamics of the cortex are reported to work near a critical point or phase transition of chaotic dynamics, known as the edge-of-chaos, representing a boundary between stability and chaos. Transitions away from this boundary disrupt cortical information processing and induce a loss of consciousness. The entropy of the electroencephalogram (EEG) is known to decrease as the level of anesthesia deepens. ⋯ Lyapunov exponents, correlation dimensions and approximate entropy were calculated from these electroencephalographic signals. As a result, maximum Lyapunov exponent was generally positive during sevoflurane anesthesia, and both maximum Lyapunov exponents and correlation dimensions were significantly greater during deep anesthesia than during shallow anesthesia despite reductions in approximate entropy. The chaotic nature of the EEG might be increased at clinically deeper inhalational anesthesia, despite the decrease in randomness as reflected in the decreased entropy, suggesting a shift to the side of chaotic enhancement under anesthesia.
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The study employed event-related potential (ERP), time-frequency analysis, and functional connectivity to comprehensively explore the influence of male's relative height on third-party punishment (TPP) and its underlying neural mechanism. The results found that punishment rate and transfer amount are significantly greater when the height of the third-party is lower than that of the recipient, suggesting that male's height disadvantage promotes TPP. Neural results found that the height disadvantage induced a smaller N1. ⋯ These results imply that the height disadvantage causes negative emotions and affects the fairness consideration in the early processing stage; the third-party evaluates the blame of violators and makes an appropriate punishment decision later. Our findings indicate that anger and reputation concern caused by height disadvantage promote TPP. The current study holds significance as it underscores the psychological importance of height in males, broadens the perspective on factors influencing TPP, validates the promoting effect of personal disadvantages on prosocial behavior, enriches our understanding of indirect reciprocity theory, and extends the application of the evolution theory of Napoleon complex.