{'fraction_non_alphanumeric': 0.025257249766136577, 'fraction_numerical': 0.0, 'mean_word_length': 6.181208053691275, '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}}
Anxiolytic drug targets: beyond the usual suspects.

Individuals suffering from anxiety experience an unpleasant emotional state defined by psychological and physiological responses to the anticipation of real or imagined danger. Physical manifestations include increased heart rate, altered respiration, sweating, trembling and fatigue, while psychological concomitants include feelings of powerlessness, apprehension, and potential danger. Many effective treatments for anxiety target the primary inhibitory neurotransmitter, γ-aminobutyrate (GABA). Within the brain, there are two principal subtypes of GABA receptor complexes: GABAA and GABAB. The subunits of the pentameric GABAA receptor form a tight group enclosing a chloride channel whereby GABA activation induces channel opening and subsequent influx of chloride ions (Cl–) into the intracellular medium. The increase in negative charge causes neuronal membrane hyperpolarization and a resultant inhibition of neurotransmitter release. In this way, GABA agonists can induce anxiolysis, sleep, and anesthesia.