A myelin, or ErbB3, study (McIntosh, 2009), shows that mutations resulting in NRG1/ErbB3 signaling failures causes oligodendrocyte activity to be impaired so that less "white matter" is produced resulting in a diminished "anterior internal capsule in subjects with both disorders" (p. 2) including unaffected directly-related family members of the bipolar disorder and schizophrenia subjects. This effect is assumed to be developmental, and myelin formation in "frontal lobes, continues into late adolescence and beyond" (p. 3), giving optimism that new drugs could reinforce myelination for those at risk.
This study also says that plasticity relates to myelination, and that there is myelination in adults, and hence plasticity, that may relate to schizophrenia and bipolar disorder in terms of both development and maturity.
Neurotransmitter, or ErbB4, studies have a brain-wide view with a focus on neuron and transmitter activity such glutamatergic hypofunction (Li, 2007), failures in the formation of inhibitory synapses (Fazzari, 2010), and neural development such as the "wiring" of GABA-mediated circuits (Fazzari, 2010), all in the context of schizophrenia. While a bipolar disorder can be linked to schizophrenia in the context of ErbB4 (Chong, 2007), the more detailed material on neural activity focuses on schizophrenia.
As dopamine hyperactivity is part of the schizophrenia pharmacological model (Stone, 2007), and methamphetamine is used to simulate it experimentally (Homayoun, 2008), studies concentrating on stimulants may give clues about the neural activity of schizophrenia and bipolar disorder.
The "white matter" study links myelination to plasticity, and is optimistic that new drugs may reinforce myelination (p. 4), and so raises an idea about myelination and plasticity with respect to maturity: could such drugs help the elderly retain plasticity?
These studies show similar diseases apparently caused by the same mutations, creating a causal relationship that should point to a common location for both diseases. But we find the expressions on completely different levels--the causal relationship is misleading! Still, the "neurotransmitter" studies show causal relationships linking the neural functions of bipolar disorder and schizophrenia to glutamatergic, GABAergic, and dopaminergic responses to stimulants, such as methamphetamine. These relations may help show us how the disordered neurons may affect behavior.
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.
Gever, J. (2009, January 15). Bipolar disorder and schizophrenia have overlapping genetic roots. MedPage Today
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. doi:10.1080/09540260902962180.
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 June 2007 vol. 21 no. 4 440-452