For many years lactate was considered to be a waste product of glycolysis. Data are accumulating that suggest that lactate is an important energy substrate for neurons during activation. In severe traumatic brain injury (TBI) glutamate release and ischemic cerebral blood flow (CBF) are major factors for a mismatch between energy demand and supply and for neuronal cell death.
View Article and Find Full Text PDFA 55-year-old woman presented with a right trigeminal dysfunction (dysesthesia) initially, followed by right oculomotor and abducens paresis lasting 1 month. Neuroimaging studies showed an enhanced mass in the right cavernous sinus extending to the trigeminal ganglion. The extraparenchymal tumor located around the right trigeminal ganglion was totally removed, except for an intracavernous lesion, by the orbitozygomatic approach.
View Article and Find Full Text PDFChemical preconditioning with low dose of 3-nitropropionic acid (3-NPA) prolongs the latency to hypoxic depolarization (HD), which triggers cell death, and also restores the synaptic transmission which disappears during hypoxia in gerbil hippocampal slices. Here we show that these neuroprotective effects are mediated by the activation of K(ATP) channels. Diazoxide, a K(ATP) channel opener, prolonged the latency to HD dose-dependently to the same extent as that of the chemical preconditioning with 3-NPA.
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