Not necessarily, perhaps just the opposite. Whatever made the person
vulnerable (the diathesis part) may still be present. Besides, this research
is relatively young.

On Sun, Jul 24, 2011 at 3:54 PM, William Scott <[email protected]> wrote:

>
>
>
>
>
> If this were true, wouldn't we expect depression not to recurr after
> termination of a thorough anti-depressant medication treatment? The data
> seem to show otherwise.
>
> Bill Scott
>
>
> >>> Carol DeVolder ** 07/24/11 12:45 PM >>>
>
>
>
>
>
> This is kind of a long post, and many of you will not be interested in it
> at all (maybe nobody), but this is in response to the discussion of
> antidepressants, depression, its potential causes, and so on. I'm not
> turning it in for a grade, so please don't grade me on it. I hope it is
> somewhat coherent though, because I really like all of the possibilities for
> explanation that emerge in this model. In a previous post, I mentioned
> Robert Julien’s *Behavioral Pharmacology* as an excellent resource. Of
> course I don’t think he has the final word on the topic of depression and
> antidepressants, I do think he provides valuable insight. Paraphrasing what
> he has to say on the topic (paraphrasing liberally, I might add, so don’t
> fault me for plagiarism—I already know that I am doing that), starting with
> the pathophysiology of depression, Julien describes what he refers to as the
> neurogenic theory of depression.
>
>
>
> This description describes depression as related to loss of volume (due to
> neuron loss), especially in the hippocampus.  Julien points out that
> numerous symptoms of depression such as impaired attention, concentration,
> and memory are related to functions of the hippocampus or the prefrontal
> cortex. He also notes that chemicals such as cortisol can have deleterious
> effects on the functioning of the hippocampus and prefrontal cortex(tying
> together the research that suggests that stress can result in loss of brain
> volume, especially in these areas). According to research by Frodl et al.
> (2007), the hippocampus actually shrinks when exposed to a variety of
> stressors, including depression. That same research reports that stress is
> one of the most common causes of depression.
>
>
>
> However, Julien notes that recent research has shown that existing neurons
> are able to repair or remodel themselves (plasticity), and in fact
> neurogenesis also is possible; again, especially in the hippocampus, but
> also in the prefrontal cortex. According to his explanation, two known
> second messenger neurochemicals  are important in protecting neurons from
> damage due to trauma or injury, and in promoting and maintaining the health
> and stability of newly generated neurons. Julien argues that antidepressants
> increase the action of these 2nd messenger systems resulting in repair and
> restoration of volume to the hippocampus and possibly the prefrontal cortex.
>
>
>
> Here’s a stepwise summary of how these 2nd messengers might act in the
> presence of SSRIs /SNRIs or other antidepressants:
>
>
>
> Step 1:  Antidepressant drugs increase the level of the monoamines
> (especially 5-HT and NE) in  the synapse.
>
> Step 2: binding of either 5-HT or NE triggers a 2nd messenger system  that
> uses  cAMP (cyclicAMP).
>
> Step 3: cAMP triggers the expression of CREB (cAMP
> response-element-binding protein).
>
> Step 4: CREB activates the production of BDNF (brain-derived neurotrophic
> factor)
>
> Step 5: BDNF promotes healthy neurons and connections (likely involving
> the growth of new  neurons, especially in the hippocampus).
>
>
>
> Julien supplies ample references to support these statements. Also, Julien
> writes that the time frame in which all of these steps occur might explain
> the therapeutic lag that accompanies the onset of administration of
> antidepressants and the onset of their therapeutic effect.
>
>
>
> If you’ve read this far, hopefully I’ve shown the possibility that
> depression may be due to stress (loss of a loved one, job loss, ongoing
> factors), chemical imbalance (genetic or acquired), or the interaction of
> any or all of these factors (the diathesis-stress model). Although
> antidepressants may alleviate depression under this model, other things can
> as well; for example, psychotherapy, exercise, self-help, stress-reduction
> techniques, or time.
>
>
>
> Some references:
>
> Angelucci, F., et al. (2005).  BDNF in schizophrenia, depression, and
> corresponding animal models. *Molecular Psychiatry* 10, 345-352.
>
> Blendy, J. A. (2006). The role of CREB in depression and Antidepressant
> treatments. *Biological Psychiatry, 59,* 1144-1150.
>
>
>
> Duman R. S. and Monteggia, L. M. (2006). A neurotrophic model for
> stress-related mood disorders. *Biological Psychiatry, 59* , 1116-1127.
>
>
>
> Frodl, T. et al. (2007). Association of the brain-derived neurotrophic
> factor Val66Met Polymorphism with reduced hippocampal volumes in major
> depression. *Archives of General Psychiatry, 64*, 410-416.
>
>
>
> Nair, A., and Vaidya, V. A. (2006). CyclicAMP response element binding
> protein and brain-derived  neurotrophic factor: Molecules that modulate
> our mood? *Journal of Bioscience, 31, *423-434.
>
>
>
> Done for the day--going outside as soon as it stops raining.
>
> Carol
>
>
>
>
> --
> Carol DeVolder, Ph.D.
> Professor of Psychology
> St. Ambrose University
> 518 West Locust Street
> Davenport, Iowa  52803
> 563-333-6482
>
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-- 
Carol DeVolder, Ph.D.
Professor of Psychology
St. Ambrose University
518 West Locust Street
Davenport, Iowa  52803
563-333-6482

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