Short communicationCorticosterone accelerates hypoxia- and cyanide-induced ATP loss in cultured hippocampal astrocytes
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Glucocorticoids, metabolism and brain activity
2021, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Therefore, interpretation of these results in terms of underlying mechanism is difficult, especially in the case of longer latencies between drug administration and metabolic testing (section 5). In contrast to short-term ischemia, the prolonged oxygen/glucose deprivation combined with corticosterone treatment leads to an opposed effect in cortical astrocytes (Tombaugh and Sapolsky, 1992). However, relevance of this in vitro finding for in vivo conditions has not been proven (see also Section 7.3).
Corticosteroids and perinatal hypoxic-ischemic brain injury
2018, Drug Discovery TodayCitation Excerpt :Without this adaptive mechanism, subsequent cellular swelling and necrosis would occur, triggering the inflammatory response of the host caused by release of cellular contents into the extracellular space [44]. In addition, mitochondrial dysfunction through exacerbation of hypoxia-induced ATP loss in hippocampal astrocytes gives an initial mechanism of HI-induced damage in the neonatal brain [45]. The intrinsic pathway of apoptosis is activated in HI injury, causing mitochondrial permeabilization, release of proapoptotic proteins (cytochrome c and apoptosis-inducing factor), and subsequent caspase activation [44].
Role of the pituitary-adrenal axis in granulocyte-colony stimulating factor-induced neuroprotection against hypoxia-ischemia in neonatal rats
2012, Neurobiology of DiseaseCitation Excerpt :We also show that administering dexamethasone after HI impairs development, and worsen apoptosis. These results support the hypothesis that elevated corticosteroids are detrimental to the functioning and recovery of neurons after an insult (McIntosh and Sapolsky, 1996; Tombaugh and Sapolsky, 1992). G-CSF reduced infarct volume 24 h after HI, and metyrapone similarly reduced infarct volume.
Effects of chronic stress and corticosterone on sialidase activity in the rat hippocampus
2011, Behavioural Brain Research
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We thank Desta Packan and Sheila Brooke for expert technical assistance and Dr. Kate Raley-Susman for helpful comments. Support was provided to R.M.S. by the National Institute on Aging (AG06633) and by a Presidential Young Investigators Award, and to G.C.T. by a pre-doctoral fellowship from the National Science Foundation.