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Re: what is Fos-Immunoreactivity? linkadge

Posted by Larry Hoover on December 29, 2005, at 7:11:27

In reply to Re: what is Fos-Immunoreactivity?, posted by linkadge on December 28, 2005, at 12:14:35

> I would be interested in the effect that lithium or antipsychotics could have on the effects of c-fos induced by antidepressants. So lithium has an attenuating effect on c-fos in certain situations. Is this of relavance to its mood stabalizing effect?

Do you see how you move away from the descriptive, as soon as you start considering relevance? It is tempting, even rational, to start making these hypotheses, but the science doesn't give us that. The science is in the observations....the knowledge is limited to "we observed ...." (I'm an empiricist. And, I don't even want to consider what happens to "science" when "important discoveries" turn out to be faked data. Like hydro lines cause leukemia. Not.)

I've seen too many theories come and go. Infinitely many more hypotheories (hypotheses)....

Okay, maybe not infinite. ;-)

> So parnate and bupropion seemed to consistantly increase c-fos in more areas of the brain than other antidepressants. Is this related to the propensity for these two drugs to resemble psychostimulants in certain paradigms? Would the addition of lithium or an antipsychotic reduce certain activation, would it preserve c-fos acivation in the amygdala?

You're a thinker. That's for sure. ;-)

> I wonder if deltaFosB is affected by parnate or bupropion. A member of the fos family that generally takes longer to turn on, has been linked to certain substance's addictivness.
> Linkadge

After reading your linked reference to d-fosB, I'd have to assume so. It's related to long-term potentiation, which is how the brain stores experience.

We had a long discussion about possible long-term drug effects. I don't question long-term drug effects conceptually, as they are part of the individual's experience. If we had the means, we could isolate specific permanent biochemical and genetic changes induced by exposure to any specific drug. If we had the means, we could isolate specific permanent biochemical and genetic changes induced by emotion. If we had the means, we could isolate specific permanent and genetic changes induced by thought. I think we could, if we had the means. But we don't. And all of those (and many others) are changing simultaneously. Which is which?

I'm not even sure we are born as tabula rasa (clean slates). As a matter of fact, I'm certain we're not. Absolutely convinced of it. And then we add unique experience to that. How big is infinity squared?

My concern is not seeing the forest for the trees. Heck, we can't see the tree for the bark. Heck, we can't see the bark for the cellulose. We can't see the cellulose for....I'm mangling the metaphor because I want to emphasize that virtually every piece of data about the brain that we have is scale dependent. The brain is an organ in a body. The e.g. limbic system is complex in the brain. The e.g. amygdala is a structure in the limbic system. The corticomedial group is a division of the amygdala. The nucleus medialis is cell cluster in the corticomedial group. Blah blah neuron, receptor, neurotransmitter, blah, blah, methylation, blah.

And it's a moving target.

That changes as it moves, because it moves.

Thousands (millions??) (billions??) of changes per second, accumulating for years.

And we want to link these scale-dependent data to behaviour?

Cause and effect? We're lucky to get correlation. And we even argue about that.

Just putting it out there.





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