{'fraction_non_alphanumeric': 0.02948207171314741, 'fraction_numerical': 0.024701195219123506, 'mean_word_length': 5.575916230366492, '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}}
Rapid activation of JNK and p38 by glucocorticoids in primary cultured hippocampal cells

Rapid activation of JNK and p38 and their translocation to the cell nucleus by glucocorticoids, corticosterone (Cort), and bovine serum‐conjugated corticosterone (Cort‐BSA) were studied in primary cultured hippocampal cells by using immunobloting and immunofluorescence confocal microscopy. The rapid activation occurred 5 min after stimulation and was maintained at plateau for as long as 2–4 hr; i.e., the response persisted for 2 hr after washing out the 15‐min application of Cort‐BSA. The activation occurred at a minimal concentration of 10–9 M for Cort and 10–8 M for Cort‐BSA. GDPβS blocked the activation, but RU38486, a nuclear glucocorticoid receptor antagonist, could not block the activation, indicating the involvement of the membrane‐delineated receptor in this reaction. The protein kinase C (PKC) inhibitor Gö6976 blocked the response, whereas the protein kinase A inhibitor H89 could not, implying the involvement of PKC in the intracellular signal transduction pathway. The nongenomic nature of the responses and the transduction pathway and the significance of persistent action and biological significance are discussed. © 2005 Wiley‐Liss, Inc.