First, your paper is an excellent one, so I am just going to focus on the last sentences of your discussion, where you propose this feed-forward loop between stress and the inhibition of adult hippocampal neurogenesis (AHN). Secondly, for the record, this is my own personal opinion on the topic and it does not imply to any extent that it is shared by any other author of the paper(s) I am going to mention (or is it quote, in a blog too?).

Coming to the discussion points you highlighted, I fell the “How could so few adult-born neurons regulate the HPA axis? “ question is the most trivial (or obvious, I should say) one, because it is a point that could be made to every single paper that tries to deal with adult neurogenesis and its functional implications. Whatever thing these “newborn cells” are meant to do (if any, because that is still questionable, of course) they do it in their “fewness”. Perhaps they are “nodes” within hippocampal circuits? It is one of the theories but, who knows?
So I will better focus on the other two points, as follows:
Do new neurons sense/detect stress through glucocorticoids?
As you discussed, although we still can not rule out indirect effects of the glucocorticoids on AHN (possibly trough glutamatergic pathways) or even less, AHN-independent effects on behavior, we have recently published a paper (http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2012123a.html) where we provide reasonably strong evidence that newborn “neurons”, or at least a fair subset of them, (actually neuroblasts) do sense GC levels directly through the glucocorticoid receptor (GR). Further, when we removed the GR from them, the cells displayed a very interesting repertoire of morphological and physiological changes, suggesting that the GR is a key player in their (correct?) functional and morphological integration. Lastly, these changes were paralleled by impaired contextual freezing during fear conditioning, suggesting again a link to behavior (see previous discussion point).
So I would say, yes, they do sense HPA activity (directly) and this activity influences AHN, consistent with your observations (and those of others of course, whose work I won’t intend to review here but it could be a nice topic for a future post of yours?).

So finally, we come to the last (and most interesting, I find) discussion point: what is that HPA activity does to these cells? Or in your words:
Is a feed-forward cascade plausible?
This is to me the most difficult to digest of your conclusions, not because I don’t like (I love it, actually) but because, as we discuss in our Commentary in Mol Psych (see Lucassen et al in your post), it seems largely unsubstantiated by the previous literature.
What do I actually mean by that? Well, the general concept in the stress field seems to be, as far as I understand it, that the effects of stress on AHN even when strong and chronic, may be largely reversible (see as a simple example Suppressed proliferation and apoptotic changes in the rat dentate gyrus after acute and chronic stress are reversible. Heine VM, Maslam S, Zareno J, Joëls M, Lucassen PJ. Eur J Neurosci. 2004 Jan;19(1):131-44.).
So the question seems to be how to incorporate your feed-forward loop concept into these previous observations. It is a challenging questions and I would be very interesting in hearing your thoughts about it.
From my side, one possibility is that although proliferation recovers, in each one of these cycles of inhibition of AHN induced by high glucocorticoids, the cells develop some sort of “cellular adaptive memory” that helps them to develop a “ type of programming (that) could be adaptive, predisposing animals to behave in ways best suited to the severity of their particular environments” as you propose in your article.
Does that sound plausible enough to you? Interested? I will be presenting some of our new data that provide some preliminary experimental support for these ideas in the SFN nanosymposium 720 “Postnatal Neurogenesis: Regulation and Temporal/Spatial Patterns” @ room 273 on October 17 Wed from 8 – 11:30 a.m., so you and everyone else interested in the discussion is welcome to be there.
Take care,
Carlos.