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Silly researchers.

Posted by Questionmark on October 7, 2003, at 12:53:04

In reply to Seen this a lot, posted by Eddie Sylvano on October 5, 2003, at 15:22:43

Great thread, people. Some really good points.
First i wanted to mention something in response to zeugma. You said "Maybe certain AD's stimulate nicotinic receptors- bupropion and nortriptyline- these are two that help smokers come off their habit." i wonder if some do. i'm not sure about others, but i know that bupropion is a nicotinic ANtagonist, which is why it's helpful for smokers-- cuz it prevents the nice/buzzlike/pleasureable effects of smoking (nicotine). i'd love to find a nicotinic agonist though-- one that works a little longer than nicotine and has a little fewer side effects.
But i really wanted to comment on the theory that antidepressants are effective primarily through increasing nerve growth factor and neuronal regeneration/growth in the hippocampus. i think this theory is extremely presumptuous. i mean, it certainly doesn't seem like increased neuro-regeneration in the hippocampus would be a bad thing, and i imagine it would be quite a good thing. But to say that it's the primary means by which antidepressants exert their antidepressant effects is a big stretch, in my opinion. i believe that the enhanced neuronal growth in the hippo. is a RESULT, or beneficial EFFECT, of the positive action/s that antidepressants have on mood and such (the neurochemical mechanisms involved in mood and such). Certainly the presence of cortisol and other stress hormones and chemicals are often highly elevated in depression, and this is believed to be detrimental to the hippocampus in particular. But i believe that the reduction in cortisol (and other "bad" stuff) from antidepressants is a secondary effect-- again, a result of the beneficial effects the drug has on the biochemical mechanisms of mood. This reduction in cortisol and what have you is probably then the main cause of increased hippocampal regrowth. Sure then this effect probably has some beneficial qualities, but i believe they are subsequent to the other effects mentioned. i don't get scientists and researchers sometimes. Just because the increase in hippocampal cell growth does not occur until a few weeks or so
after starting an antidepressant, and this is relatively the same as when antidepressants start to exert their beneficial effects, does NOT mean that the latter is caused by the former. Wouldn't it be just as reasonable to assume that the former is a result of the latter?? i bet you if/once they ever do make drugs that directly increase NGF or neuronal regrowth in the hippocampus, it will have a very limited effect on depression. i very well could be wrong (and i hope i am, i think), and they could be right, but even so i think it is quite presumptuous for them to make this theory such a strong option at this point. For one thing, if they're wrong many of us will have gotten our hopes up for nothing. But i'll stop rambling now.
Oh wait, and yeah, i think that's a really good question that Eddie asked about how scientists can gauge depression in a rat. Two ways i'm aware of in which they do this is by 1) measuring/comparing activity in different rats (physical activity and movement, etc.), and 2) through the forced swim test. This is basically when they drop a rat in a bucket of water it can't get out of and they measure how long it can swim for. i've read about this test being used in so many studies it's ridiculous. Besides sounding incredibly cruel, how much can you seriously freaking associate depression with how long a rat can swim in a bucket? i'm just a dumb undergraduate, so maybe i'm missing something, but it always amazes me how much researches over-assume and presuppose. This further makes me question the validity of the antidepressants-work-by-increasing-neuron-regeneration-in-the-hippocampus theory. Okay, sorry, i'll seriously stop rambling now.


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poster:Questionmark thread:265309
URL: http://www.dr-bob.org/babble/20031004/msgs/266382.html