| Topic: |
Sociology > Depression |
| User: |
"Charles" |
| Date: |
30 Jun 2007 04:12:56 AM |
| Object: |
depression and stress and neurogenesis |
bits and pieces from this web site:
http://www.biopsychiatry.com/newbraincell/index.html
Many scientists believe that stress is the most significant causal
agent--with the possible exception of genetic predisposition--in the
etiology of depression. In addition, nerve cells in the hippocampal
formation are among the most sensitive to the deleterious effects of
stress. Consequently, a stress-induced decrease in neurogenesis in the
hippocampus might be an important factor in precipitating episodes of
depression. On the other hand, increasing serotonergic
neurotransmission is the most effective treatment for depression, and
it also augments hippocampal neurogenesis. So serotonin-induced
increases in neurogenesis might promote recovery from depression.
Considering all of this, we suggest that the waning and waxing of
neurogenesis in the hippocampal formation might trigger the
precipitation of and recovery from episodes of clinical depression.
Utilizing the brain imaging technique of MRI, Yvette Sheline and her
colleagues at Washington University in St. Louis reported smaller
hippocampal volumes in a group of older women with recurrent major
depression. Although the subjects were in remission, they had smaller
left and right hippocampal volumes--but comparable total cerebral
volumes--in comparison with carefully selected controls. Sheline’s
group also found a significant negative correlation between total days
of depression and the volume of the left hippocampal gray matter. The
investigators speculate that this hippocampal loss might result from
glucocorticoid-induced neurotoxicity associated with recurrent
episodes of depression. In a more recent study, this same group
confirmed their original report and also showed that the decrease in
hippocampal volume correlated with total lifetime duration of
depression and not with age. Other studies confirm the relationship
between depression and hippocampal volume. For example, Premal Shah
and his colleagues at the Royal Edinburgh Hospital also reported
smaller hippocampal volumes in chronically depressed patients but
found no decrease in hippocampal volume in recovered patients.
The clinical benefit of drugs that increase serotonergic
neurotransmission encouraged one of the authors (Jacobs) to test
fluoxetine (Prozac), which increases brain levels of circulating
serotonin by inhibiting it from being taken back into neurons that
release it. We gave adult rats a three-week, systemic treatment of
fluoxetine and found an approximately 70-percent increase in the
number of cells produced in the dentate gyrus. Ronald Duman’s group at
Yale University confirmed and extended that result. They found that
fluoxetine, antidepressants acting preferentially on norepinephrine
and chronic electroconvulsive shock all increased cell proliferation
in a rat’s dentate gyrus.
And from this site:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=60045
More challenging, what are the cellular bases of the persistent
atrophy? Some plausible candidate mechanisms exist, all built around
the numerous ways in which major depression is, ultimately, a
stress-related disorder.
In the broadest statement of what the current study suggests,
administration of antidepressants not only can cure the affective
symptoms of depression, but also can reverse some disquieting
neurobiological correlates of depression as well.
A number of studies using rodents indicate that some of the standard
treatments for depression, namely administration of antidepressant
drugs or the use of electroconvulsive therapy, have effects on the
hippocampus that should counter those reported in major depression.
For example, one class of antidepressant drugs prevents stress-induced
retraction of dendritic processes (12, 13). In addition, both
antidepressant drugs and electroconvulsive therapy increase adult
neurogenesis in the hippocampus (14, 15)
Charles
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| User: "Cyberhive" |
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| Title: Re: depression and stress and neurogenesis |
30 Jun 2007 05:47:21 AM |
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