Two manuscripts appear in this issue of Biological Psychiatry involving suicide. Ernst et al. (1) found reduced expression of connexin 30 and connexin 43, which regulate calcium transients in the lateral prefrontal cortex of suicide completers. It is thought that astrocytes express connexins and it is argued that altered connexins affect astrocyte function, which could contribute to suicide. Cyprien etal. (2) found that the size of the caudal third of the corpus callosum was reduced in a group of suicide attempters. Taken together, the findings support the notion that there may be a neurobiology of suicide distinct from the psychiatric disorders commonly associated with suicide, involving alterations in glia, white matter, and by extension, the regions where the astrocytes are derived from (1) and where the regions contribute fiber tracts to the corpus callosum (2). Given the markedly different substrates (astrocytes vs. white matter; prefrontal cortex vs. corpus callosum), there is the further likelihood that suicide neurobiology has multiple phenotypes involving not only neurodegeneration but also neuro-developmentand neuroplasticity.
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