https://www.selleckchem.com/pr....oducts/2-hydroxybenz
Experimental studies have indicated that prolonged ketamine exposure in neonates at anesthetic doses causes neuronal apoptosis, which contributes to long-term impairments of learning and memory later in life. The neuronal excitotoxicity mediated by compensatory upregulation of N-methyl-d-aspartate receptors (NMDARs) is proposed to be the underlying mechanism. However, this view does not convincingly explain why excitotoxicity-related apoptotic injury develops selectively in immature neurons. We proposed that the GABAA recep
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