Posted by zeugma on June 11, 2006, at 14:50:25
In reply to Re: Klonopins relationship to serotonin » zeugma, posted by SLS on June 11, 2006, at 11:46:14
Because of how cognitively affected and mentally slowed I am. I have almost no short-term memory. It is as if my executive functions have been dampened or poorly stimulated. I also display a "deficit syndrome" that probably involves hypoactiviy in limbic areas. I was wondering if there were hypoactive limbic afferents to the DLPFC that might not be stimulating that area enough. Perhaps it is the other way around. Maybe a hypoactive DLPFC fails to stimulate reward centers. Maybe deficiencies in the LC fail to stimulate the DLPFC directly or indirectly.>>
The DLPFC has a particular connection with spatial memory, and DLPFC lesions compromise performance on any task that requires maintainance of spatial information (for example, humans with DLPFC lesions would be unable to find their way through an airport). The DLPFC is also, as you know, deactivated during REM sleep, and dreams are processes in which one 'loses one's way.' (It is a selective deactivation because the other areas of the cortex are still active, although without NE or 5-HT inputs.) Of the various drugs I have taken, modafinil most strongly activates the 'dorsal pathway,' which is involved in determining where an object is. Methylphenidate by contrast is best for various forms of agnosia, such as a difficulty with facial recognition and difficulty perceiving colors: this is the 'ventral' pathway (determining 'what' an object is). Of note, methylphenidate is MUCH better with anhedonia and other 'negative' symptoms (the striatum is ventral to the PFC). I am only speaking of my own experience though it tallies with the literature.
The problem with all this is that researchers are able to report on the effects of particular lesions or manipulations of neurotransmitters, but the interactions between all the systems are not known, although manipulating one system produces change in all.
I'm not sure if any of this is helpful. The formula I have here in front of me- that striatal D2 stimulation produces cognitive flexibilty, while PFC D1 stimulation produces cognitive stability- seems far too simple. What do you think?
-z
poster:zeugma
thread:654917
URL: http://www.dr-bob.org/babble/20060610/msgs/655535.html