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Hippocampal Function

kenneth Collins kpaulc at earthlink.net
Mon Jan 3 12:06:08 EST 2000


dag.stenberg at helsinki.nospam.fi wrote:
> 
> Brian Scott <brians at interlog.com> wrote:
> > I don't have the reference here but this group used the standard
> > bromodeoxyuridine techniques for measuring cell division along with
> > cell-type markers to show an increase in neurogenesis following
> > administration of several antidepressants as well as ECS.  I think
> > Druganow was one of the authors but I'm not sure.  I think their point
> > was that neurogenesis may underlie some of the antidepressant effects of
> > these treatments.
> 
> Now we are getting somewhere.
> In abstract 283.16, Barry Jacobs (B.L.Jacobs, a wellknown top serotonin
> expert) and C.A. Fornal report "Chronic fluoxetine treatment increases
> hippocampal neurogenesis in rats: a novel theory of depression".
> 
> They do in the abstract explain their reasoning (which certainly
> stimulates thought and discussion, thanks to you for pointing it out to
> me), and as it does not get any better by my trying to extract,
> I will cite the abstract in extenso:
> 
> "Last year we reported that pharmacological activation of the 5-HT1A
> receptor dramatically increased dental gyrus neurogenesis in adult rats
> and, reciprocally, that blockade of this receptor decreased spontaneous
> neurogenesis (Jacobs et al., Soc Neurosci Abstr Vol.24, Part 2, p.1998,
> 1998). Changes in brain serotonin are implicated in the etiology of
> depression, and especially in its treatment.

this last phrase is bogus be-cause the distribution of brain serotonin
is activation-'state' dependent.

that is, with respect to physically-real neural information-processing,
the action of serotonin is =completely= dependent upon convergence upon
'Type II' synchronization (AoK, Ap5).

but when serotonin precursers 'flood' the brain, elevating serotonin
levels, such is completely 'ignorant' of the necessary Type II
synchronization.

rather than constituting a 'treatment', such is analogous to introducing
spurious code in a computer program.

yes, the program will run differently, but no, such does not constitute
'better information-processing', and, in fact, most likely leads to a
diminution of the information-processing of the system, be it a
computer, or a sertonin-flooded brain.

it's a Crushing-Sorrow to see folks at the mercy of the ignorance that's
reflected in this 'treatment' premise.

there are no 'short-cuts' to convergence within neural
information-processing dynamics.

yes, flooding the brain with this or that chemical substance can 'alter'
the brain's information-processing dynamics, but what good is such if
the only thing such does is diminish the brain's information-processing
capabilities?

it doesn't 'magically' eliminate the information-processing problems
with which individuals, groups, and societies are confronted.

all it does, for the sake of 'feeling-good', is assure that the
information-processing problems with which individuals, groups, and
societies are confronted will =not= be solved.

the ignorance involved constitutes a real threat to Humanity's
going-forward.

one can see the negative effects of already-widely-distributed
psychoactive substances without even trying to.

'leaders' ho-humming their ways through their daily affairs,
substituting drug-induced 'side-stepping' for actual problem-solving.

society-wide, the effects of such are cummulative.

Sadly, the main 'target' of the 'drugs' seems to be "Conscience", with
folks on the 'drugs' being transformed into _Mad Magazine's_ "Alfred E.
Newman"... "What? Me worry?"

there're no 'short-cuts'.

all of this is discussed in AoK, BTW, which, i understand, is one of the
'reasons' AoK has been Censored.

K. P. Collins

> In particular, 5-HT1A
> receptor activation appears to be especially important therapeutically
> (for a recent brief review, see Koek et al.  J. Pharm Exp Ther
> 287:266-283, 1998). Because of this involvement of serotonin in adult
> neurogenesis, we decided to examine the effects of the prototypic
> antidepressant drug, fluoxetine, on neurogenesis. Adult Sprague-Dawley
> rats (5/group) were administered fluoxetine HCl (5 mg/day i.p.) or
> saline for 21 days and for the final 7 days were also given
> bromodeoxyuridine (BrdU; 100 mg/kg ip.) 30 min later. Animals were
> killed 14 days later and their brains processed for BrdU
> immunohistochemistry. Chronic administration of fluoxetine produced a
> significant 70% increase (p=0.015) in the number of BrdU lebelled cells.
> These data in conjunction with a variety of other basic and clinical
> data suggest that dentate gyrus neurogenesis may be a critical element
> in the onset of, and recovery from, depression in humans. We hypothetize
> that the onset of depression, for example that due to genetic
> predisposition and/or attributable to stress, may be due to decreased
> ongoing spontaneous neurogenesis. On the other hand, the recovery from
> depression may be due to an increased rate of neurogenesis caused by
> activation of the 5-HT1A receptor by any of a variety of clinically
> effective means. The time required for these newly born neurons to
> mature and be incorporated into the existing neural circuitry may
> explain the well-known 'therapeutic lag' of SSRIs and other treatments
> for depression."
> 
> - I shall have to hunt up Koek et al:s article as well.
> - It seems (from PubMed) that none of the Jacobs neurogenesis research
> is yet published, so we will have to live by the abstract so far.
> 
> Dag Stenberg




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