Motivation: I'm trying to figure out how my brain works. I definitely have bipolar tendencies (and genetic reasons to suspect so) and schizoid personality disorder, along with scoring rather highly on autism/Asperger's quizzes. I have a tendency to take more ideas more seriously than most, which I suspect for completely unrelated reasons has to do with increased neuronal excitability. I also seem to have rather high neural plasticity (I learn quickly in varied domains, update ontologies quickly, update beliefs quickly, et cetera) though it's possible that such plasticity is not abnormal among those of roughly my age and fluid intelligence. These factors led me to find the dysfunctional sodium pump hypothesis to be reasonably likely, at least in my case, but it saddens me that I don't seem to be able to easily construct a model out of the hints that Wikipedia is giving me.
Ultimately I think my intellectual productivity (and quality of life, happiness level, interestingness, et cetera) is better when I'm manic and I'd like to take advantage of that, but I feel obligated to see how Algernon's principle applies and if trying to be always-manic-schizo would significantly increase my risk of actual schizophrenia or something else bad like increased neurotoxins due to purposefully messed up sodium pump activity patterns or something unanticipated.
I may be reading between the lines too much, but I get the sense that you're not diagnosed by a psychiatrist, or undergoing treatment. If that's the case, this might not be the exact area to try to outdo the professionals.
I was looking at a hypothesis that bipolar disorder is probably due to problems with neocortical sodium-potassium pump activity cyclically decreasing and thus allowing increased resistance, which increases neuronal excitability by the square of the resistance. According to what I've read on Wikipedia it seems that agonizing Gi proteins would inhibit cAMP production and therefore downregulate sodium pump activity (this was the most tenuous part, and the reference was unintelligible) and increase neuronal excitability. But 5-HT1A (a type of Gi protein) agonists have been shown to be useful for improving symptoms of schizophrenia, which is typically thought of as resulting from increased neuronal excitability. Sign error? What's up? I don't have any model of the underlying mechanisms, and only vaguely know what words like 'downregulate' mean.
ETA: But apparently http://en.wikipedia.org/wiki/Risperidone , a 5-HT2A agonist, also supposedly mitigates symptoms of schizophrenia, which is weird because it increases neuronal excitation. It seems that the flawed assumption is that schizophrenia has something to do with 5-HT-caused neuronal excitability.
Thus it seems like maybe you can reduce bipolar tendencies by taking 5-HT1A antagonists, and schizophrenia is its own separate problem that is perhaps solved by taking a D2 antagonist. 5-HT2A agonists increase neuronal excitation which may interact somehow with the the 5-HT1A antagonists. I'm still confused.
There's this other problem where if the main reason D2 and 5-HT1A work is by decreasing neuronal excitability that might just be because sedate people are more similar to each other than manic people, but the kind of neuronal excitability that makes people manic and the kind that makes people schizoid are qualitatively different, and hence the difference in receptors being important. It could be that 5-HT2A agonists and 5-HT1A antagonists increase and decrease neuronal excitability respectively, but in different ways such that they're not countervailing.