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Background
Corticosterone is a steroid hormone produced in the cortex of the adrenal glands that binds to both glucocorticoid and mineralocorticoid receptors[1].
Corticosterone, via SGK phosphorylation of GDI at Ser-213, increases the formation of GDI-Rab4 complex, facilitating the functional cycle of Rab4 and Rab4-mediated recycling of AMPARs to the synaptic membrane. It provides a potential mechanism underlying the role of corticosteroid stress hormone in up-regulating excitatory synaptic efficacy in cortical neurons[2].[1]. Lu NZ, Wardell SE, Burnstein KL, et al. International Union of Pharmacology. LXV. The pharmacology and classification of the nuclear receptor superfamily: Glucocorticoid, mineralocorticoid, progesterone, and androgen receptors. Pharmacol, 2006, 58(4): 782-797.
[2]. Liu W, Yuen E Y, Yan Z. The Stress Hormone Corticosterone Increases Synaptic α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptors via Serum- and Glucocorticoid-inducible Kinase (SGK) Regulation of the GDI-Rab4 Complex. Journal of Biological Chemistry, 2010, 285(9): 6101-6108.
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