ABSTRACT
The concept that severe premenstrual affective, behavioral, and physical symptoms could be triggered by ovulation and the rise and fall of ovarian sex steroids in the luteal phase of the menstrual cycle was an advance over previous notions that the symptoms resulted from ‘agitated menstrual blood seeking escape from the womb’. Still, the explicit psychoneuroendocrine etiology of premenstrual syndrome (PMS) remains unknown, and more than two decades of research have demonstrated that a simple alteration of hormones, neuropeptides, or neurotransmitters cannot completely explain the occurrence of the symptoms. The purpose of this chapter is to provide an overview of the three leading hypotheses that currently attempt to explain the biological basis of PMS. To this end, we will discuss the monoamine neurotransmitter serotonin (5-hydroxytryptamine, 5-HT); the GABAergic neurotransmitter system, in particular, the GABAA receptor complex; and the pro-opiomelanocortin (POMC) pathway, in particular, the endogenous opiate peptide, -endorphin.
