{'fraction_non_alphanumeric': 0.034053700065487885, 'fraction_numerical': 0.019646365422396856, 'mean_word_length': 5.47457627118644, '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}}
GABAA Receptor Structure and Function in NT2-N Cells after Hypoxia

Hypoxia causes dysfunction of excitatory and inhibitory neurotransmission, often resulting in encephalopathy, seizures, or myoclonus. We evaluated the effects of hypoxia on γ -aminobutyric acid (GABA)A receptor (GABAAR) function and expression in an in vitro model of neuronal hypoxia. NT2-N cells, derived from the human NT2 teratocarcinoma cell line, were exposed to ≤1% O2 for 8 hours and then used immediately for experiments or allowed to recover under normoxic conditions (95% air/5% CO2) for 24, 48, or 96 hours. Hypoxic treatment did not cause obvious morphologic changes or cell death. In whole-cell patch-clamp recordings, the GABA current median effective concentration (EC50) was unchanged; however, maximal GABA-evoked currents changed in a biphasic manner. Maximal GABA currents were significantly increased immediately after hypoxia, but were significantly reduced after 48-hour normoxic recovery, and then returned to baseline after 96-hour recovery. Maximal potentiation of 10 μM GABA currents by diazepam was increased 48 hours after hypoxia, but potentiation by zolpidem was decreased. Barbiturate enhancement and zinc inhibition of GABA currents were unchanged. Semiquantitative reverse transcriptase (RT)polymerase chain reaction (PCR) showed decreased α1, α5, β2, and γ 2 subunit mRNA after hypoxia. Hypoxic exposure altered GABAAR physiology and subunit mRNA expression, which may correlate with symptoms observed after hypoxia in vivo.