You mentioned that stress can functionally inhibit the degree of
neurogenesis within the hippocampus. That is not entirely true. There has
been some studies that have shown that acute stressogenic conditions can
facilitate the genesis of newly created granule cells from progenitor cells
in the SVZ regions. Even, as of yet unpublished work from some of my
colleagues, have shown a similar trend. For example, an acute exposure to a
mild 10-min. cold water immersion stressor will increase hippocampal
neurogenesis, as inferred by BrdU labeling (a method that does have some
methodological issues as you are probably familiar). Interestingly enough
no one has considered whether the newly generated neurons in fact express
any glucocorticoid based receptors, either GR or MR (i have proposed that
this might be faciliated through IGF-1 signalling, since this system has
been considered to be important for eliciting hippocampal neurogenesis). I
have generally advocated that this acute stressor and accompanied
neurogenesis may in fact be a compensatory mechanism against the deleterious
actions elicited by prolonged de-regulation of the HPA axis. So perhaps it
isn't stress, per se, but instead the duration of the stressor that may have
the paradoxical action upon neurogenesis. Needless to say I don't find that
any bit surprising considering the fact that prolonged stress elevates
cortisol (corticosterone in rats) levels to a point that functional
suppression of the immune response occurs. That is why stress and the
development of cancer go so hand in hand. I would be interested if you
could cite any studies that showed acute stress inhibiting neurogenesis.
Perhaps the type of stressor activates different aspects of the HPA system
to produce differential actions upon neuronal functioning. (there are
numerous examples of this idea within neuronal-based communication... I
wouldn't be surprised if this occurring here).
NMF
----- Original Message -----
From: "Matthew Kirkcaldie" <Matthew.Kirkcaldie at newcastle.edu.au>
Newsgroups: bionet.neuroscience
Sent: Sunday, September 07, 2003 8:02 PM
Subject: Re: Prozac and Neurogenisis
> In article <3f598c5c at dnews.tpgi.com.au>,
> "John H." <john at faraway.com.au> wrote:
>> > As to ssris and neurogenesis, my spin on that is as serotonin levels
rise
> > the HPA axis is modified reducing cortisol levels, the dentate gyrus is
very
> > high in GC receptors and neural progenitor cells v. sensitive to
> > glucocorticoids. Thus the delay in ssri efficacy may relate to this slow
> > turning down of excessive cortisol production, which is one of the most
> > frequently reported aspects of depression.
>> Interesting call - after all, we do know that stress decreases
> neurogenesis, and I recently saw a talk describing glucocorticoid
> mechanisms in hippocampus which were of possible relevance to your idea
> there.
>> I still think there is a strong argument to be made in favour of the DG
> turnover contributing to behavioural integration, though - have a look
> at the Kempermann review from last year (if you can stomach the irksome
> computer analogies).
>> Cheers,
>> Matthew.
