Evidence for alterations of the glial syncytium in mood disorders
Medina A, Thompson RC, Burke S, Bunney WE, Myers RM, Schatzberg AF, Barchas JD, Akil H, Watson SJ
Society for Neuroscience. 2012.
Astrocytes are a glial cell type that provides packing and sustenance for neurons and play a pivotal role in neurotransmission. A principal characteristic of these glial cells is their ability to function as a syncytium, creating a very active functional apparatus that regulates and maintains homeostasis of the brain parenchyma. Astrocytes are extensively interconnected by gap junctions. This allows them to perform spatial buffering, a distribution process where the accumulation of small molecules produced by neural activity can be diffused to the adjacent glia and then be dispersed to more distal components of the glial syncytium, restoring neural tissue to its basal condition. Several molecules are involved in the syncytial activity of astrocytes, including ion channels, water channels, protein complexes associated with them and gap junction hemichannels. In this study we used microarray technology to investigate the integrity of the glial syncytium in major depression disorder (MDD) patients. Fresh frozen blocks of human hippocampus from MDD and control subjects were obtained from the Brain Donor Program at the University of California, Irvine. The blocks were cut using a cryostat into 10 μm sections that where then anatomically aligned to select homologous levels of the hippocampus for microarray analysis. Laser capture microdissection was used to collect the tissue and samples were processed using Illumina Human HT-12 v4.0 arrays (illumina Inc, Hayward, CA). Control versus disease expression differences were assessed using differential scores and Student’s t-test.
Microarray results showed that diverse constituents of the glial syncytium are altered in MDD, including water channels and their associated molecules, gap junction components and potassium channels. In conclusion, glial syncytium dysfunction may play an important role in the pathogenesis of MDD.