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liu, J.

Publications and source records attributed to liu, J..

3 recordsLinked to original sources

Fronto-temporal structural alterations in congenital aphantasia

Congenital aphantasia is characterized by a lifelong self-reported absence of voluntary visual imagery despite preserved visual knowledge, offering a natural model for dissociating sensory representation from conscious imagery. Functional imaging evidence suggests that this dissociation may arise from altered top-down interactions between higher-order control systems and high-level visual cortex, but its structural correlates remain unknown. Here, using diffusion and structural MRI in 18 individuals with congenital aphantasia and 18 matched visualisers, we tested two competing accounts of aphantasia: one predicting structural differences in visual pathways, the other predicting differences in higher-order associative networks. Across multimodal analyses of white-matter tract microstructure, functional-ROI tractography, graph-theoretic network organization, and cortical morphometry, aphantasia was associated with structural differences in frontotemporal and cingulate white-matter tracts, including the uncinate fasciculus, posterior interparietal callosal fibres, and dorsal cingulum, and in frontotemporal cortical regions, including the anterior insula, anterior prefrontal cortex, and medial temporal cortex, together forming a candidate neuroanatomical signature for the broad cognitive-affective profile of aphantasia. By contrast, we found no reliable group differences in early visual cortex, major visual tracts, or the direct structural connections of the core imagery network. Congenital aphantasia therefore exhibits a pattern of structural alterations centered on frontotemporal and cingulate systems, sparing the principal visual pathways. Given the modest sample size, these findings are exploratory and hypothesis-generating and require replication in larger cohorts; they nonetheless suggest that higher-order systems supporting integration and conscious access, rather than visual representations themselves, may contribute to the absence of conscious imagery in congenital aphantasia.

neuroscience↗

Spatiotemporally selective ATP events from astrocytes encode injury information and guide sustained microglial response

Brain injuries, either directly result from external assaults or are accompanied with diseases, initiate a cascade of intrinsic responses for damage management, with resident microglia as one of the key responders in the early phase of reaction. Changes in microglia including their motility and activities can be tuned according to injury intensity and position, indicating such injury information is precisely encoded and actively presented. Also, microglia in a broad area can perform sustained migration towards a transient and local injury, suggesting a signal amplification process may exist that bridge differences between injury and microglial migration in time and space. Currently, the molecular identity and underlying mechanism for injury encoding, amplification and presentation have not been fully elucidated yet, although candidate molecules like ATP are linked with both injury and microglial response. Based upon our recent technique advancement in engineering novel genetically-encoded ATP sensors, we here identified and characterized that in the cortex of awake mice in vivo, a new type of spatiotemporally selective ATP events, referred to as Inflares, was selectively evoked after brain injuries, which were actively and repeatedly generated from astrocytes in a Ca2+-dependent manner through the opening of pannexin 1 channel. Functionally, Inflares amplified local injury over time and space with their persistence and widespread distribution, and provided continuous directionality that was necessary for guiding microglial migration. Excessive Inflares in pathological injuries drove microglial dysfunction and caused secondary damage, whereas blocking Inflares successfully reversed pathological changes and benefited the outcome of ischemic stroke. Together, we identified the internal mechanism that encoded and presented injury information, and provided rational target for treating injury-related diseases.

neuroscience↗

A warmer growing season triggers earlier following spring phenology

Under global warming, advances in spring phenology due to the rising temperature have been widely reported. However, the physiological mechanisms underlying the warming-induced earlier spring phenology remain poorly understood. Here, using multiple long-term and large-scale phenological datasets between 1951 and 2018, we show that warmer temperatures during the previous growing season between May and September led to earlier spring phenology in the Northern Hemisphere. We also found that warming-induced increases in maximum photosynthetic rate in the previous year advanced spring phenology, with an average of 2.50 days {degrees}C-1. Furthermore, we found a significant decline in the advancing effect of warming during the previous growing season on spring phenology from cold to warm periods over the past decades. Our results suggest that the observed warming-induced earlier spring phenology may be driven by increased photosynthetic carbon assimilation in the previous season, while the slowdown in the advanced spring phenology arise likely from decreased carbon assimilation when warming exceeding the optimal temperatures for photosynthesis. Our study highlights the vital role of photosynthetic carbon assimilation during growing season in spring phenology under global warming.

ecology↗