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Poursadegh, A.

Publications and source records attributed to Poursadegh, A..

2 recordsLinked to original sources

A population readout of extrastriate activity reveals biased and smoothed temporal representations across saccades

Perception of visual time is transiently distorted around saccadic eye movements, yet the neuronal mechanisms constructing perisaccadic representations of time remain unclear. Here, we investigate how perisaccadic temporal information is encoded and read out in extrastriate cortex, by combining electrophysiological recordings in V4 and MT neuronal population in macaque monkeys under high spatiotemporal resolution visual stimulation, and a statistical modeling framework capturing perisaccadic response modulations at single-trial precision. Our analyses show that perisaccadic neuronal responses systematically shift the temporal representation of presaccadic stimuli within receptive fields-biasing them toward earlier times, and also reduce temporal sensitivity for presaccadic stimuli-impairing discrimination of stimulus onset times. Model-based readout using time-varying spatiotemporal sensitivity maps in neuronal ensembles enables quantitative characterization of these effects and identifies their specific neuronal response components at millisecond resolution. In silico manipulations further demonstrate a causal role of representational bias in reducing temporal sensitivity. These findings suggest that extrastriate cortex implements an active encoding strategy to stabilize presaccadic temporal information by favoring the most recent reliable input, revealing a fundamental tradeoff between temporal precision and robustness that supports a continuous visual percept across saccades. This finding also establishes a general role for extrastriate populations in constructing the perception of visual time.

neuroscience↗

Spontaneous onset of cellular markers of inflammation and genome instability during aging in the immune niche of the naturally short-lived turquoise killifish (Nothobranchius furzeri)

Turquoise killifish (Nothobranchius furzeri) are naturally short-lived vertebrates, recapitulating several aspects of human aging, including protein aggregation, telomere shortening, cellular senescence, and declined antibody diversity. The mechanistic causes of systemic aging in killifish are still poorly understood. Here we ask whether killifish undergo significant age-dependent changes in the main hematopoietic organ, which together could contribute to systemic aging. To characterize immune aging in killifish, we employed single-cell RNA sequencing, proteomics, cytometry and a functional in vitro assay. Our data indicate how old killifish display increased inflammatory markers, and while immune cells from adult killifish display increased markers of proliferation and replication-independent DNA repair in progenitor-like cell clusters, progenitors from old killifish display extensive markers of DNA double-strand breaks. In less than 10 weeks, killifish undergo several dramatic spontaneous aging-related changes in the immune niche, which could be functionally linked with its extensive systemic aging and serve as targets for anti-aging interventions.

immunology↗