{'fraction_non_alphanumeric': 0.016142735768903994, 'fraction_numerical': 0.0, 'mean_word_length': 5.848837209302325, '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}}
Role of the γ‐Aminobytyric acid receptor—Ionophore complex in seizure disorders

The possibility of a role for the inhibitory neurotransmitter γ‐aminobutyric acid (GABA) in seizure disorders has been strengthened by biochemical studies showing that various nervous system depressant drugs can modulate GABA receptor binding in vitro. In particular, two classes of anticonvulsant agents, the benzodiazepines and the barbiturates, have modulatory receptor sites on the GABA receptor‐ionophore protein complex of the postsynaptic membrane. Furthermore, it is well established that direct block of GABA function causes seizures and that augmentation of GABA function can protect against seizure activity. Direct evidence for altered GABA synaptic markers has been obtained in some animal models of epilepsy, as well as in human focal epilepsy. We present preliminary evidence for a deficit in benzodiazepine receptor binding in the midbrain of seizure‐susceptible Mongolian gerbils. These data would be consistent with an impairment of GABA‐mediated inhibitory synaptic transmission that contributes to susceptibility to the genesis or spread of seizures in some kinds of epilepsy.