Posted by SLS on September 14, 2006, at 12:11:09
In reply to Re: Glutamatergic neurotransmission and mood disor, posted by linkadge on September 14, 2006, at 11:39:36
> Another thing to consider is this. Persons with a family history of unipolar depression often show atrophy in the prefrontal cortex. So even under the most ideal conditions, the frontal cortex might be in a state of hypofunction. In this case, you've got certain drugs that can boost activity there. While they are not curing the atrophy, they may restore some ballance that may not be otherwise achievable.
> So perhaps the hippocampus is hypfunctioning as a result of prefrontal hypofunction. In which case directly targeting the hippocampus may
> not completely restore normal behavior.I tend to agree with this scenario. There is a positive feedback loop between the cortex and the hippocampus for which the frontal cortex must remain functional in order for the whole system to operate properate properly. I have, in the past, considered hippocampal hypofunction and atrophy to be secondary to the primary pathology of mood illness - whatever that is. I can now see how it becomes a contributor towards a worsening course of illness once it is initiated.
http://bjp.rcpsych.org/cgi/content/full/177/5/402/FIG1
- Scott
poster:SLS
thread:685302
URL: http://www.dr-bob.org/babble/20060909/msgs/685903.html