Neuroscience
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The myelination of axons, which is performed in brain tissues by specialized glial cells (oligodendrocytes) is crucial for correct formation of the complicated neural circuitry necessary for normal cognition, sensation, and motor function. Myelin-related anomalies are seen in many neurodegenerative diseases and in psychiatric disorders, including major depressive disorder and post-traumatic stress disorder. ⋯ In this article, after brief review of published data on myelin abnormalities in stress-related psychiatric disorders, we focus on recent cellular and molecular discoveries in various rodent models including models of chronic unpredictable stress, social isolation stress, chronic social defeat stress, and chronic immobilization stress. We also attempt to compile and analyze currently scarce data on myelin-related impairments resulting from early postnatal stress.
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Astrocyte dysfunction, and in particular impaired extracellular potassium spatial buffering, has been postulated to have a potential role in seizure susceptibility and ictogenesis. Inwardly rectifying potassium (Kir) channels, and specifically KIR4.1, have a predominant role in K+ homeostasis and their involvement in neuronal excitability control have been hypothesized. To avoid the severe side effects observed in Kir4.1 cKO, we studied the effects of Kir4.1 down-regulation in cortical astrocytes by using Kir4.1 RNA interference (RNAi) technique combined with in utero electroporation (IUE) at E16 and a piggyBac transposon system. ⋯ Intriguingly, immunohistochemical analysis performed on slices studied with electrophysiology revealed a reduced number of neurons generated from radial glial cells in Kir4.1- rats. We conclude that focal down-regulation of Kir4.1 channel in cortical astrocytes by Kir4.1 RNAi technique combined with IUE is not effective in altering potassium homeostasis and seizure susceptibility. This technique revealed a possible role of Kir4.1 during corticogenesis.
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Sodium tanshinone IIA sulfonate (STS) can protect against brain damage induced by stroke. However, the neural protection mechanism of STS remains unclear. We investigated whether STS performs its protective function by suppressing autophagy and inflammatory activity during brain injury. ⋯ STS treatment reduced neuroinflammation, as assessed by the infiltration of macrophages and neutrophils, corresponding with reduced numbers of macrophages, T cells, and B cells in ischemia/reperfusion (I/R) brains. In addition, STS treatment also attenuated the upregulation of autophagy associated proteins, such as LC3-II, Beclin-1 and Sirt 6, which was induced by MCAO. These results demonstrated that STS can provide remarkable protection against ischemic stroke, possibly via the inhibition of autophagy and inflammatory activity.