Neurosteroids are steroids de novo synthesized in the brain or metabolized in situ by blood borne precursors. Neurosteroids influence brain function via both genomic and nongenomic mechanisms ; the first include the induction of progesterone receptors in cultured oligodendrocytes, the latter include the modulation of calcium channel and of chloride channel opening. Some neurosteroids act as GABA-A agonists, such as allopregnanolone and tetrahydrodesoxycorticosterone; others are GABA-A antagonists, such as DHEA and pregnanolone sulfate (Figure 1). Brain is the first known source of neurosteroids. Bixo et al. have evaluated women post-mortem concentrations of allopregnanolone in brain cortex, amygdala, hippocampus, caudate nucleus, putamen, thalamus, and the highest levels were observed in the substantia nigra and basal hypothalamus . The regional differences in brain steroid levels imply different local mechanisms for steroid uptake and binding. Brain concentrations of allopregnanolone were significantly higher in fertile women at luteal phase than in postmenopausal controls; this may depend on ovarian steroid production, indicating that the secretion pattern during the menstrual cycle is reflected in the brain . A5 androgens have also been measured in specific regions of cadaver brains and the central/plasmatic ratio of DHEA demonstrated a higher concentration of the steroid within the brain [1,3].
KeywordsAnorexia Nervosa Luteal Phase Premenstrual Syndrome Neuroactive Steroid Fertile Woman
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