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Current hypotheses regarding the pathophysiology of anxiety disorders emphasize an imbalance between neuronal excitation and inhibition, characterized by reduced Gamma-aminobutyric acid (GABA) inhibition and excessive glutamatergic activity, which contributes to neuronal hyperexcitability and the manifestation of anxious behaviors (111)

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Its primary mechanism of action is the upregulation of brain-derived neurotrophic factor (BDNF), a protein that supports neuronal survival, synaptic plasticity, and the formation of new neural connections