{'fraction_non_alphanumeric': 0.017045454545454544, 'fraction_numerical': 0.001893939393939394, 'mean_word_length': 5.732484076433121, '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}}
Ketamine Treatment Translocates Gsalpha from Lipid Rafts in Cultured Glial Cells: Similar Effects to Several Antidepressant Compounds

Previous studies have demonstrated that all classes of monoamine‐centric antidepressants increase coupling between the G protein, Gsalpha and adenylyl cyclase, resulting in sustained cAMP production. This effect requires sustained drug treatment and is observed after 3 days in cultured neural or glial cells or 3 weeks in rats. This is apparently due to Gsalpha being released from constraints of a lipid raft environment to cholesterol‐poor regions of the plasma membrane. Consistent with this, both peripheral tissue and postmortem brain from depressed human subjects show a greater proportion of Gsalpha in lipid rafts. In an effort to determine whether the “glutamate‐centric” ketamine showed an antidepressant “biosignature” similar to other antidepressants, studies in cultured cells were initiated. It was hypothesized that ketamine would have an effect similar to antidepressants but along a shorter time course.