Neuroscience
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Humans and non-human primates are known to lengthen their response time (RT) to a go signal when they occasionally must cancel their responses following a stop signal in a countermanding task as well as to adjust their RT adaptively on a trial-by-trial basis. Less is clear regarding the adaptive RT adjustments in the countermanding performance of rodents. To investigate this question, male Wistar rats (N=12) were trained with food reward to press a lever directly below an illuminated light (go signal), but to countermand the lever press subsequent to a tone (stop signal) presented infrequently (25% of trials) at variable delays. ⋯ RT lengthening following erroneous stop trials was observed in sessions with a 10-s TO interval, but not with a 1-s TO interval. Analyses of RT distributions suggest that RT lengthening results largely from reduced sensitivity to the go signal, but also from reduced readiness. These findings indicate that rats exert control in the countermanding task by lengthening RT in anticipation of stop trials to avoid long, unrewarded TO intervals.
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Infants that succumb to Sudden Infant Death Syndrome (SIDS) have been identified with inner ear dysfunction (IED) at birth and on autopsy. We previously investigated whether IED could play a mechanistic role in SIDS. We discovered that animals with IED displayed significant suppression of movement arousal to a hypoxic-hypercarbic gas mixture under light anesthesia. ⋯ This contrasts with other studies that have identified hypercarbia as an arousal stimulus with EEG. Further studies are warranted to evaluate the precise role of the inner ear in the movement response and potential association with SIDS. The early detection of IED in SIDS predisposed cases could be invaluable.
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Antisocial personality disorder (ASPD), one of whose characteristics is high impulsivity, is of great interest in the field of brain structure and function. However, little is known about possible impairments in the cortical anatomy in ASPD, in terms of cortical thickness (CTh) and surface area (SA), as well as their possible relationship with impulsivity. In this neuroimaging study, we first investigated the changes of CTh and SA in ASPD patients, in comparison to those of healthy controls, and then performed correlation analyses between these measures and the ability of impulse control. ⋯ In addition, we also found that the ability of impulse control was positively correlated with CTh in the SFG, MFG, orbitofrontal cortex (OFC), pars triangularis, superior temporal gyrus (STG), and insula cortex. To our knowledge, this study is the first to reveal simultaneous changes in CTh and SA in ASPD, as well as their relationship with impulsivity. These cortical structural changes may introduce uncontrolled and callous behavioral characteristic in ASPD patients, and these potential biomarkers may be very helpful in understanding the pathomechanism of ASPD.
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Illusory conjunctions (e.g. the confusion between the shape of one stimulus with the color of another stimulus) are the most dramatic expression of binding failures in vision. Under brief exposure or when attention is diverted illusory conjunctions may be observed in healthy participants, but they only represent a real-life problem for patients with parietal damage. However, it is unclear whether such failures reflect the impairment of early or late stages of visual processing. ⋯ In contrast, when presentation was bilateral she either identified the correct right shape-color combination and missed the item in the left hemifield (extinction) or combined incorrectly the right shape with the left color (illusory conjunction). Evoked potential analyses revealed a specific electrophysiological signature of illusory conjunctions, starting ∼105ms after stimulus onset over the right frontal cortex. These findings indicate that binding errors reflect failures of early stages of attentional filtering relying on the integrity of the posterior parietal cortex.
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G protein-coupled receptors (GPCRs) are involved in many fundamental cellular responses such as growth, death, movement, transcription and excitation. Their roles in human stem cell neural specialization are not well understood. In this study, we aimed to identify GPCRs that may play a role in the differentiation of human embryonic stem cells (hESCs) to neural stem cells (NSCs). ⋯ CXCR4 agonist SDF-1 promoted, whereas the antagonist AMD3100 delayed the neural induction process. In consistence with antagonizing CXCR4, knockdown of CXCR4 in hESCs also blocked the neural induction and cells with reduced CXCR4 were rarely positive for Nestin and Sox1-staining. Taken together, our results suggest that CXCR4 is involved in the neural induction process of hESC and it might be considered as a target to facilitate NSC production from hESCs in regenerative medicine.