PMC:6891830 / 5212-6054 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/6891830","sourcedb":"PMC","sourceid":"6891830","source_url":"https://www.ncbi.nlm.nih.gov/pmc/6891830","text":"Histological studies in the mice revealed a novel combination of astrocytic changes. Western blot studies demonstrated a modest increase in glial fibrillary acid protein, but no evidence of astrocyte proliferation. This is notable, as astrocyte proliferation typically follows more severe focal brain injuries.4 Animals with mild TBI, however, exhibited patches of cortex with reduced immunostaining for several astrocytic markers, including glutamate transporter 1 (Glt1), glutamine synthetase, the inward rectifier potassium channel Kir4.1, and the gap junction channel protein connexin43 (Cx43). Cell counts and cell death measures support the conclusion that astrocytes are still present in these patches but have developed phenotypic changes in protein expression. 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