Sex steroids-induced neurogenesis in adult brain: a better look at mechanisms and mediators

Abstract

Adult neurogenesis is the production of new nerve cells in the adult brain. Neurogenesis is a clear example of the neuroplasticity phenomenon which can be observed in most of mammalian species, including human beings. This phenomenon occurs, at least, in two regions of the brain: the subgranular zone of the dentate gyrus in hippocampus and the ventricular zone of lateral ventricles. Numerous studies have investigated the relationship between sex steroid hormones and neurogenesis of adult brain; of which, mostly concentrated on the role of estradiol. It has been shown that estrogen plays a significant role in this process through both classic and non-classic mechanisms, including a variety of different growth factors. Therefore, the objective of this review is to investigate the role of female sex steroids with an emphasis on estradiol and also its potential implications for regulating the neurogenesis in the adult brain.

Longterm Increased S100B Enhances Hippocampal Progenitor Cell Proliferation in a Transgenic Mouse Model

“…Although BDNF levels in brain tissue may fluctuate in the postnatal period dependent on the brain region and species, in general, levels decrease with age. Furthermore, BDNF expression is affected by sex steroids [ 45 ], and critically involved in the regulation of age-related processes in the hippocampus, including neurogenesis and neuronal plasticity [ 30 ]. Since ApoE may positively modulate BDNF expression [ 24 ], it would be interesting whether the decreased hippocampal ApoE levels in male S100Btg mice found in our study were accompanied by altered BDNF.…”

Reproducible stability of verbal and spatial functions along the menstrual cycle

“…However, the estradiol peak is notoriously hard to capture resulting in high rates of data exclusions, which has prompted researchers to center their hypotheses around the luteal cycle phase. However, estradiol and progesterone have opposite effects on various neurophysiological processes, including neurogenesis [ 33 ], synaptogenesis [ 34 ] and a plethora of neurotransmitter systems [ 35 ] and also demonstrate interactive effects, e.g., by estrogen priming of progesterone receptor synthesis [ 36 ]. Accordingly, significant findings during the luteal phase cannot be attributed exclusively to estradiol, progesterone, or interactive actions, and null findings do not necessarily preclude ovarian hormone effects because progesterone and estradiol actions may cancel each other out.…”