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FROM NEUROINFLAMMATION TO BEHAVIOR: UNCOVERING MICROGLIA ROLE IN PERINATAL STROKE
Emanuela Berettaand 5 co-authors
University of Padua
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-039
Presentation
Date TBA
Board: PS05-09AM-039
Event Information
Poster Board
PS05-09AM-039
Poster
View posterAbstract
Perinatal ischemic stroke, occurring between the 20th gestational week and the 28th postnatal day, affects about 1 in 2,300 live births and overlaps with critical windows of heightened plasticity.
By disrupting neurodevelopmental trajectories, the injury induces neuronal death and triggers microglia, the resident immune cells in the brain. While microglia-driven inflammation is associated with detrimental outcomes in adulthood, their role in the developing brain after early-life injury remains poorly understood. To tackle this challenge, we induced a cortical lesion by permanent middle cerebral artery occlusion (MCAO) on postnatal day (P)14 and assessed spontaneous recovery by longitudinal behavioral testing (2–79 days post-injury). MCAO mice revealed motor deficits in the grid walk test, associated with a core lesion volume of about 2.5 mm³ and a reduction in neuronal population (NeuN⁺ cells). To dissect the specific contribution of microglia, we depleted this population via a 5-day treatment with the CSF1R inhibitor, PLX-5622, reducing Iba1+ cells by 85%.
By disrupting neurodevelopmental trajectories, the injury induces neuronal death and triggers microglia, the resident immune cells in the brain. While microglia-driven inflammation is associated with detrimental outcomes in adulthood, their role in the developing brain after early-life injury remains poorly understood. To tackle this challenge, we induced a cortical lesion by permanent middle cerebral artery occlusion (MCAO) on postnatal day (P)14 and assessed spontaneous recovery by longitudinal behavioral testing (2–79 days post-injury). MCAO mice revealed motor deficits in the grid walk test, associated with a core lesion volume of about 2.5 mm³ and a reduction in neuronal population (NeuN⁺ cells). To dissect the specific contribution of microglia, we depleted this population via a 5-day treatment with the CSF1R inhibitor, PLX-5622, reducing Iba1+ cells by 85%.
Beyond immune surveillance, microglia also regulate synaptic pruning and circuit maturation, crucial for excitatory–inhibitory (E/I) balance. We therefore analyzed stroke-induced reorganization by quantifying excitatory (vGLUT–PSD95) and inhibitory (vGAT–Gephyrin) pre- and post-synaptic markers, and perineuronal nets (PNNs), under microglia modulation.
Finally, to integrate central and systemic inflammation, we collected peripheral blood from the same animals to correlate circulating inflammatory markers with microglial activity and functional outcomes. Altogether, our findings will shed light on microglia role in neuroinflammation, synaptic remodeling and neuroimmune crosstalk in the developing brain, providing a foundation for potential therapeutic strategies.
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