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Premenstrual syndrome (PMS) is a clinical condition characterized by a recurrent pattern of physical, emotional, and behavioral symptoms that emerge during the luteal phase of the menstrual cycle and typically resolve within a few days of the onset of menses [PMID: 30855866]. While not a single molecular target, the pathophysiology involves the complex interaction between cyclic ovarian steroids (estrogen and progesterone) and central neurotransmitters, particularly serotonin and gamma-aminobutyric acid (GABA) [PMID: 21359561]. Allopregnanolone, a metabolite of progesterone, acts as a potent positive allosteric modulator of GABA-A receptors, and its fluctuating levels are thought to contribute to mood instability in sensitive individuals [PMID: 24703529]. Therapeutic strategies focus on stabilizing these hormonal fluctuations using oral contraceptives or addressing the secondary neurochemical imbalances using selective serotonin reuptake inhibitors (SSRIs) [PMID: 31034451]. PMS serves as an indication for various drug classes, but it is considered an incorrect term for a specific protein or receptor target in a molecular biology context.
Modulation of serotonin levels via serotonin transporter (SERT) inhibition; suppression of the hypothalamic-pituitary-ovarian axis to prevent hormonal fluctuations; inhibition of cyclooxygenase (COX) to reduce prostaglandin-mediated pain; and antagonism of mineralocorticoid receptors to reduce fluid retention [PMID: 30855866, PMID: 21359561].
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