Jin et al. investigate the neurovascular impact of microinfarcts, revealing transient neural suppression with minimal cell death and recovery linked to vascular remodeling. Fast-spiking interneurons exhibit reduced excitability, whereas regular-spiking neurons showed increased bursting activity. Disruptions in low-gamma phase locking suggest persistent network instability. These findings underscore the subtle, yet lasting impairments caused by a single microinfarct.
Abstract
Microinfarcts, the “invisible lesions”, are prevalent in aged and injured brains and associated with cognitive impairments, yet their neurophysiological impact remains largely unknown. Using a multimodal chronic neural platform that combines functional microvasculature imaging with spatially resolved neural recording, the neurovascular effect of a single microinfarct is investigated. Unlike larger strokes, microinfarcts induced only temporary suppression of neural activity with minimal cell death, with recovery paralleling vasculature remodeling at the infarct core. Neural activity is more severely suppressed at the shallower cortical layer despite milder vascular damage compared to deeper layers, and the excitability of fast-spiking interneurons attenuation is accompanied by heightened bursting of regular spiking neurons. Spike phase locking at the low-gamma band is disrupted, indicating a lasting impairment of long-range assembly communication. These results highlight the subtle yet significant neurovascular disruptions of a single microinfarct.
Advanced Science, EarlyView. Read More
