Posted by tealady on January 18, 2006, at 23:06:30
In reply to Re: FAT gene linked to Bipolar disorder, posted by nolvas on January 18, 2006, at 21:24:03
> Also linked to depression as well it seems. The modern diet appears to have less Omega 3 fatty acids now and more Omega 6.
>
> http://www.medicalnewstoday.com/medicalnews.php?newsid=25134
>
>
Hi Nolvas,
I wondered how the heck they worked out the rats were depressed.. some may have just been pretending to look happy ;-) sooo I clicked on the link.
The manuscript for the Journal of Lipid Research paper can be downloaded from the following URL: jlr.org/cgi/content/abstract/C500003-JLR200v1.this one.. and you get that the depressive rats were fed the same diet, but they were different type of rat, namely FSL rats.
hmm ...maybe they have a something different about these rats anyhow that causes the fats to have a difference balance in their brains..
googles FSL rats
http://www.biopsychiatry.com/flinders.htmThe Flinders Sensitive Line (FSL) rats were originally selectively bred for increased responses to an anticholinesterase agent. The FSL rat partially resembles depressed individuals because it exhibits reduced appetite and psychomotor function but exhibits normal hedonic responses and cognitive function. The FSL rat also exhibits sleep and immune abnormalities that are observed in depressed individuals. Neurochemical and/or pharmacological evidence suggests that the FSL rat exhibits changes consistent with the cholinergic, serotonergic, dopaminergic, NPY, and circadian rhythm models but not the noradrenergic, HPA axis or GABAergic models of depression. However, evidence for the genetic basis of these changes is lacking and it remains to be determined which, if any, of the neurochemical changes are primary to the behavioral alterations. The FSL rat model has been very useful as a screen for antidepressants because known antidepressants reduced swim test immobility when given chronically and psychomotor stimulants did not. Furthermore, rolipram and a melatonin agonist were shown to have anti-immobility effects in the FSL rats and later to have antidepressant effects in humans. Thus, the FSL rat model of depression exhibits some behavioral, neurochemical, and pharmacological features that have been reported in depressed individuals and has been very effective in detecting antidepressants.
So I dont know.
How did they selectively bred these rats?It doesn't seem that they function exactly the same as depressed people and yet it appears they screen anti-D's on them?
I know we just can't test on humans.... but
still the ARE saying they've found in this rat bred to appear to have some things the same as people when depressed.. I've never swum long anyway without giving up! and I reckon I'd have a high degree of immobolity if asked to swim ashore a long distance off a island..
So these rats DO have more arachidonic acid and no more (n-3 PUFA, or saturated and monounsaturated FAs. So maybe if you have more AA you have a high degree of immobility in a swim test?,http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8455816&dopt=Abstract
again something about "like depressed humans, it is supersensitive to the behavioral and hormonal effects of cholinergic (muscarinic) agonists"
Can anyone explain that bit to me.. wondering if we should avoid choline etc.
Jan
poster:tealady
thread:600472
URL: http://www.dr-bob.org/babble/alter/20051208/msgs/600575.html