User talk:Rachel Francon

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Where there are deficits of one kind or another (whether genetic or caused by blockage of the MR receptors by Spironolactone, the ongoing spiraling effects of chronic stress leadingto depression are most likely the result of the role of aldosterone action on the MR Receptors being strongly implicated in the enhancement of neurogenesis. This may be direct or it may be indirect as the spiraling stress and its cortisol will lead to apoptosis of neurons as well diminution of neurogenesis via aldosterone action at the now blocked MR receptors.

The differnetiation and mobilization of new neural cells in the areas of the Brain most strongly implicated in depression and anxiety is in the Amygdala and the Hippocampus and that is where the preponderance of MR receptors is. The relation of the use of some anti-depressants to enhanced BDNF production may be considered consistent with this neurogenesis related causation of depression via the shift in balance from aldosterone action at the MR receptor to Glucocorticoid action at that receptor with dosages of Spironolactone. The shift in balance of the MR/GR ration is also a shift in balance in the neurogenesis/apoptosis ratio. . For full discussions of the role of neural progenitor cells as part of the depression caused by Spironolactone which are more recent since the emergence of stem-cell related awareness see Francon or  Kino)

What are the pmids for the reviews in question and which review supports which content? Also what is with all the capital letters? Doc James (talk · contribs · email) 02:29, 23 November 2015 (UTC)