this section is an implementation of annotated bibliography that (eventually) hopes to blend referential support, footnotes, and (most important) forum discussion with the idea that it is our differing influences that define our points of view, and that by combining these influences we should come to agreed-upon explanations for phenomena
A look back on this research shows how abstracted this simplified model is, and the size of the gap between pure science and everyday reality. Initially I intended to directly apply the research which links many diseases to a single signalling error, but resistance from experts in the field forced me to reduce this one error to a single disorder, psychosis, because (as they say) psychosis is functionally related to bipolar, but not to schizophrenia. In defense of the pure scientists, the signalling goes to "maintenance" cells such as the astrocyte in the background. (I think of these cells as relatives of neurons).
A though that occurred to me as I first read the studies, is that I had once hypothesized that the fat on the cells, mylein, gets burned off when the mind is over active, such as in the term "burned out." This occurred to me in the mid-90s when I was fixing an expensive desktop computer and noticed that the CPU chip got much hotter when it was running a "batch job" than when it was still. Given the many abstracted similarities between computers and humans, I also assumed human intellectual matter will get hotter in similar proportions, and hence "burn off" the insulation causing dysfunction--in any part of the brain. This implicates both dopamine-exciting meth, and extreme overactivity caused by, say, terror-level fear resulting in trauma, sometimes called an insult.
Chong, V., Thompson, M., Beltaifa, S., Webster, M., Law A., and Weickertad, S. (2007). Elevated Neuregulin-1 and ErbB4 protein in the prefrontal cortex of schizophrenic patients: Schizophr Res. 2008 March ; 100(1-3): 270–280. doi:10.1016/j.schres.2007.12.474.
Fazzari, P., Paternain, A., Valiente, M., Pla, R., Luján, R., Lloyd, K., et al. (2010). Control of cortical GABA circuitry development by Nrg1 and ErbB4 signalling. Nature, 464(7293), 1376-1380. doi:10.1038/nature08928.
Homayoun, H., & Moghaddam, B. (2008). Orbitofrontal cortex neurons as a common target for classic and glutamatergic antipsychotic drugs. Proceedings of the National Academy of Sciences of the United States of America, 105(46), 18041-18046. doi:10.1073/pnas0806669105.
Li, B., Woo, R., Mei L., Malinow, R., (2007, May 24). The neuregulin-1 receptor ErbB4 controls glutamatergic synapse maturation and plasticity. Neuron, 54(4), 583-597.
McIntosh, A., Hall, J., Lymer, G., Sussmann, J., and Lawrie, S. (2009). Genetic risk for white matter abnormalities in bipolar disorder. International Review of Psychiatry, 21(4), 387-393. doi:10.1080/09540260902962180.
McIntosh, A., Hall, J., Lymer, G., Sussmann, J., and Lawrie, S. (2009). Genetic loading for psychosis and the internal capsule disorder. International Review of Psychiatry, 21(4), 387-393.
Stone, J., Morrison, P., and Pilowski, L. (2007, January 26). Review: Glutamate and dopamine dysregulation in schizophrenia — a synthesis and selective review. Journal of Psychopharmacology. 21(4), 440-452