Moderate Hypobaric Hypoxia Modifies Ca2+-Mediated Glutamatergic Signal Transduction in Rat Cerebral Cortex

Abstract

Examination of fluorescent Ca(2+)-responses to stimulation by ionotropic glutamate receptor agonists in rat cerebral cortex slices, preconditioned with hypobaric hypoxia, has demonstrated different time course for up-regulation of their Ca(2+)-conductivity and for stimulation of the consequent binding of the Ca(2+) which entered the cell. The evident result is the development of AMPA-mediated moderate increase of intracellular Ca(2+).

Effect of Ca2EDTA on Zinc Mediated Inflammation and Neuronal Apoptosis in Hippocampus of an In Vivo Mouse Model of Hypobaric Hypoxia

“…The relative contribution of signaling cascades in mediating neuronal damage hold the key to development of effective therapeutic strategies against hypobaric hypoxia-induced neuronal injury. Glutamate mediated calcium excitoxicity and subsequent neurodegeneration is associated with memory dysfunction on exposure to hypobaric hypoxia [2] , [15] . Recently, it has been indicated that zinc, which is co-localized and released along with glutamate, might induce neurophysiological alterations similar to calcium [16] .…”