With regard to the first possibility, ADX results in massive death of mature granule cells in the dentate gyrus (Sloviter et al., 1989; Gould et al., 1990). Replacement of ADX rats with aldosterone, a mineralocorticoid that binds with high affinity to MRs, is sufficient to protect the dentate gyrus from cell death (Woolley et al., 1991), suggesting that regular activation of MRs is important for normal dentate gyrus function. These findings suggest that dying mature granule cells may provide signals that stimulate the proliferation of progenitor cells. In this regard, it is relevant to note that direct destruction of the dentate gyrus, via chemical or mechanical lesion, leads to an increase in the production of new neurons (Gould & Tanapat, 1997). The link between cell survival and cell proliferation has not been extensively explored in the dentate gyrus but several reports suggest that neuronal death can stimulate adult neurogenesis in many other brain regions, including the neocortex and striatum (Gould, 2007). It is possible that dying cells produce a chemical signal that is mitogenic. Alternatively, mature intact neurons may provide
