Decreased prefrontal CaMKII α mRNA in bipolar illness

Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) plays critical roles in neurotransmission, synaptic plasticity, learning and memory. The aim of this study was to examine, by in situ hybridization, prefrontal cortical expression of CaMKII α mRNA in postmortem brains of unipolar, bipolar, schizophrenic, and control subjects. Compared to controls, bipolar patients had significantly lower levels of CaMKII α mRNA in laminae I-VI of Brodmanns area 9 and laminae I-III and VI of area 46. Unipolar patients also exhibited significantly lower levels of CaMKII α mRNA in laminae I-IV of area 9 than did controls. The significant decrease in CaMKII α mRNA in bipolar patients could be associated with some of the affective and cognitive alterations that have been linked to prefrontal cortical dysfunction in bipolar disorder, although this requires further direct examination.