Glial-associated changes in the cerebral cortex after collagenase-induced intracerebral hemorrhage in the rat striatum

• Published in: Brain research bulletin Vol. 134; pp. 55 - 62
• Main Authors: Neves, J.D., Aristimunha, D., Vizuete, A.F., Nicola, F., Vanzella, C., Petenuzzo, L., Mestriner, R.G., Sanches, E.F., Gonçalves, C.A., Netto, C.A.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.09.2017
• Subjects: Animals; Cellular events; Cerebral Cortex - pathology; Cerebral Cortex - physiopathology; Cerebral Hemorrhage - pathology; Cerebral Hemorrhage - physiopathology; Collagenases; Corpus Striatum - pathology; Corpus Striatum - physiopathology; Cortex; Disease Models, Animal; Disease Progression; Forelimb - physiopathology; Glial changes; Glial Fibrillary Acidic Protein - metabolism; Hemorrhagic stroke; Male; Motor Activity; Movement Disorders - pathology; Movement Disorders - physiopathology; Muscle Strength; Neuroglia - pathology; Neuroglia - physiology; Rats, Wistar; S100 Calcium Binding Protein beta Subunit - metabolism; Striatum; Striatum; Glial changes; Cellular events; Hemorrhagic stroke; Cortex
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/j.brainresbull.2017.07.002

•Sensorimotor cortex is susceptible to the striatal hemorrhagic injury.•Striatal ICH causes glial changes in the cerebral cortex with similar patterns and evolution as those in the striatum.•Glial effects are associated to lesion progression and functional sensorimotor outcome. Striatum and the cerebral cortex are regions susceptible to secondary injury after intracerebral hemorrhage (ICH) and glial cells in tissue adjacent to the hematoma may modulate cellular vulnerability after brain damage. Nonetheless, while the glial- associated changes occurring in the cerebral cortex after ICH may be important in maximizing brain recovery, they are not fully understood. The aim of this study was to evaluate the temporal profile of glial-associated changes in the cerebral cortex after ICH. First, the motor consequences of ICH and its relation to the lesion volume were analyzed. Secondly, glial cell proportion (GFAP+ and S100B+ astrocytes, CD11+ microglia) in the ipsilesional sensorimotor cortex and striatum, using flow cytometry were evaluated. ELISA was used to measure GFAP and S100B content in these structures as well as S100B levels in serum and cerebral spinal fluid. Main results revealed that ICH induced a delayed increase in GFAP+ cells in the sensorimotor cortex, as compared to the striatum, although the pattern of GFAP expression was similar in both structures. Interestingly, the time-curve patterns of both S100B and CD11+ microglial cells differed between the cortex and striatum. Altogether, these results suggest a different dynamics of glial-associated changes in the cerebral cortex, suggesting it is a vulnerable structure and undergoes an independent secondary process of reactive glial plasticity following intracerebral hemorrhage.