{'fraction_non_alphanumeric': 0.02391304347826087, 'fraction_numerical': 0.0010869565217391304, 'mean_word_length': 5.873134328358209, '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}}
Sustained NMDA receptor activation by spreading depolarizations can initiate excitotoxic injury in metabolically compromised neurons

•  Spreading depolarization (SD) is a profound neuronal and glial depolarization implicated in the progression of acute brain injury. •  In metabolically compromised tissue, SD can trigger irrecoverable injury; however, the underlying cellular mechanisms are not well established. •  We investigated consequences of SD in hippocampal brain slices, using a combination of electrophysiological and single‐cell imaging methods. •  We characterized a brief period of prolonged NMDA receptor (NMDAR) activation after SD onset, which appeared to underlie extended Ca2+ elevations in dendrites. •  Prolonged NMDAR activation was sufficient to cause injury after SD in metabolically compromised neurons, and therefore may contribute to deleterious consequences of SD in pathological conditions.