{'fraction_non_alphanumeric': 0.025547445255474453, 'fraction_numerical': 0.009124087591240875, 'mean_word_length': 5.535714285714286, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Excitotoxic brain damage in the rat induces interleukin‐1β protein in microglia and astrocytes: Correlation with the progression of cell death

Interleukin‐1 beta (IL‐1β) has been proposed as a mediator of several forms of brain damage, including that induced by excitotoxins. In vitro studies suggest that glial cells are the effector cells of IL‐1β‐mediated neurodegeneration. We have investigated the expression of IL‐1β protein by glial cells in vivo in response to NMDA receptor‐mediated excitotoxicity in the rat parietal cortex and striatum.