Most of the original neuroreceptor research (including theories about dopamine and serotonin uptake) was derived from backwards reasoning: psychiatric medications were studies for their efficacy and mechanism, and it was discovered that the neuroleptics (e.g., phenothiazines, such as stelazine, thorazine, haldol, prolixin, etc) dampened the effectiveness of neurotransmitters, making neural tissue less responsive to dopamine. From this it was hypothesized that, therefore, the people who "need" the medication must have too much dopamine or must be too sensitive to it.
Some initial research on mental patients seemed to support this hypothesis.
There were some problems with the underlying logic, though. First off, "schizophrenia" (that still-hypothetical brain disease diagnostically known only by its subjectively interpreted behavioral symptoms) is not a thorazine deficiency disease. Second, the population on which the original research was performed consisted in large part of long-term patients who had been taking neuroleptic medication for years before the research had been conducted.
Well, gee, if I made you take something that dampened your system's responsiveness to something it needs, then took you off it long enough to do some research a few years later, I'd probably find your tissues hyperresponsive at that point, too, due to compensation effects!
I don't know the state of the research and knowledge base at this point, but I have a sense that it is still common for test populations of "schizophrenics" to include people who have been taking psych medications over a long period and/or who are taking it during the course of the studies.
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OTHER PROBLEMS ENDEMIC TO PSYCHIATRIC RESEARCH
It is still common for research that includes behavioral outcome assessments to NOT be double-blind (i.e., researchers know the schizzies from whatever control group they are using at all times, assuming there even exists a control group of non-schizzies); and, if the research revolves around the use of pharmaceuticals, vitamins, dietary components, etc., the psychiatrists, psych nurses, or researchers are often aware of who is taking the substance under consideration, and in many cases so are the patients themselves (they may not be informed of the particulars but they know if their 'meds' have been changed or not).
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All in all, though, I associate dopamine, and the ability of the neurons to fire easily with little resistance, with a tendency to think "outside the box", to have a good imagination, but also to have a tendency to connect up ideas and thoughts that aren't associated in any meaningful sense, or to jump "off-track" from one line of thought to another as if they fed into each other when they do not, and, in particular, to think metaphorically and at times to have trouble distinguishing between metaphorical representation of a thought or idea and the thought or idea itself.
LSD and other psychedelics tend to nudge the brain in the easy-firing direction, and these psychoactive chemicals were once called "psychotomimetic" under the theory that they mimic the experiences of psychosis. But that viewpoint fell out of vogue some time ago in the study of psychoactive compounds, or so I think I recall.
All in all, the psychiatric researchers have been barking up the neurotransmitter (esp. dopamine) tree for several decades now with little concrete to show for it, so it may be the wrong tree. (An inability to DEFINE schizophrenia in a manner that can successfully survive a double-blind trial is part of the problem!!!). But they may nevertheless be on to something.
Original SDMB thread - What does it feel like to have schizophrenia?
See my previous post on this same thread