From Synapse to Symptom: Understanding Panic Attacks in Women through Neurotransmitter and Receptor Pharmacology

Background: Panic attacks are acute, sudden episodes of fear and autonomic arousal that disproportionately affect women. This heightened vulnerability is associated with hormonal fluctuations, neurotransmitter dysregulation, and receptor-level sensitivity in key brain regions.  Objective: To explore the neurochemical, receptor-mediated, and hormonal factors contributing to panic attacks in women and to examine how network pharmacology can help in identifying multi-target pharmacological strategies.  Methods: We conducted a narrative literature review on neurotransmitters (serotonin, GABA, norepinephrine, CRF), their associated receptors (5-HT1A, 5-HT2C, GABA-A, α2-adrenergic, CRF1), and their influence on brain regions like the amygdala and locus coeruleus. We also utilized network pharmacology frameworks to map compound-target-pathway relationships for drugs used in panic disorder management.  Results: Findings indicate that women with panic attacks frequently exhibit altered serotonergic and GABAergic transmission, hyperresponsive adrenergic signaling, and dysregulated HPA axis activity. Hormonal fluctuations across the menstrual cycle influence receptor function. Network pharmacology reveals interconnected pathways involving neurochemical targets and hormonal modulators, allowing for personalized therapeutic opportunities.  Conclusion: Panic attacks in women are the result of complex interactions between neurotransmitter imbalances, receptor dysfunction, and hormonal modulation. Network pharmacology provides a systems-level approach to identify new therapeutic targets and to support the development of multi-targeted, gender-specific treatments for panic disorder.