Oestrogen has clear effects on several neurotransmit-ters, including serotonin, acetylcholine, noradrenaline and dopamine. It cumulatively acts as an agonist on serotonergic function by increasing the number of serotonin receptors, serotonin (5-HT) postsynaptic responsiveness and neurotransmitter transport and uptake. It also increases serotonin synthesis and boosts the levels of the metabolite 5-hydroxy indole acetic acid (5-HIAA). It is well known that the serotonergic system plays a substantial role in regulating mood, sleep, sexual activity, appetite and cognitive ability. Serotonin is a major component in the development of depression. Our knowledge of the role of serotonin in depression has been extended into PMS research [4] and several studies demonstrated altered 5-HT metabolism in these patients. Blood levels and platelet uptake of 5-HT have been found to be low in PMDD patients, and acute depletion of trypto-phan, the precursor of serotonin, aggravates symptoms of PMS and PMDD. This hypothesis is supported indirectly by the observation that serotonin-receptor concentrations vary with changes in oestrogen and progesterone level. The well-known selective serotonin reuptake inhibitors (SSRIs) Fluoxetine, Paroxetine, Citalopram and Sertraline, have been shown to be extremely efficacious in treating severe PMS and PMDD [6]. This gives additional, albeit indirect, support to theory of involvement of serotonin in PMS aetiology.

Vitamin B6 (pyridoxine) is a cofactor in the final step in the synthesis of serotonin and dopamine from dietary tryptophan. However, no data have yet demonstrated consistent abnormalities either of brain amine synthesis or deficiency of cofactors such as vitamin B6.

Low activity of gamma aminobutyric acid (GABA) has been reported in patients with depression, PMDD and PMS. Oestrogen increases binding of GABA agonists and the upregulation of GABA receptors. In addition to the effect of SSRIs on the serotonergic system, they have been shown to enhance GABA function, hence improving depressive symptoms. Investigations of the metabolites of progesterone have shown that women with PMS had lower levels of allopregnanolone in the luteal phase

[7]. This provides another plausible theory, as allopreg-nanolone has GABA-ergic activities and its deficiency can induce symptoms similar to those experienced in PMS (Fig. 41.2).


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