Abstract TP574: Persistent Glial Activation in the Forceps Minor of Corpus Callosum is Associated With Impairment in Paired-Associate Learning

• Published in: Stroke (1970) Vol. 50; no. Suppl_1
• Main Authors: Chow, Wei Zhen, Walker, Frederick Rohan, Ong, Lin Kooi, Nilsson, Michael
• Format: Journal Article
• Language: English
• Published: 01.02.2019
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/str.50.suppl_1.TP574

Abstract only Two-thirds of stroke survivors experience cognitive impairment which reduces the quality of life by affecting the ability to return to work and social participation. Our understanding of the neuropathology of cognitive impairment post-stroke is limited, hence requires clarification in order to design interventions to improve cognitive function after stroke. We hypothesize that inflammation in one or more brain regions regulating paired-associate learning (PAL) contributes to visuospatial impairment after stroke. Focal ischemia was induced in the prefrontal cortex at the somatosensory and motor cortex using photothrombosis in eight weeks old C57BL/6 male mice. We assessed visuospatial function daily at 22 weeks post-stroke using PAL task performed on the mouse touchscreen platform (Campden Instruments Ltd, UK). Tissue loss in the medial prefrontal cortex, corpus callosum and hippocampus was calculated using Nissl-stained brain sections. Changes in neuronal, astrocyte and microglia markers were measured in the peri-infarct and associated brain regions using western blot. At 27 weeks post-stroke, stroke mice had significantly lower mean correct rate in PAL compared to sham (57.1% vs 69.1%, p=.032). Significant tissue loss was identified in the ipsilesional hemisphere and corpus callosum in stroke compared to sham. At the peri-infarct, sustained astrogliosis and neuronal loss was marked by increased expression of glial fibrillary acidic protein, and decreased mature neurons and postsynaptic density protein 95. Examination of other brain regions revealed a significant increase in the expression of CD68 and Iba1 in the forceps minor after stroke, indicating microglial activation. No changes were observed in brain regions remote to the infarct. In conclusion, we show that persistent glial activation in the peri-infarct and forceps minor of corpus callosum may be associated with visuospatial impairment following stroke.