Glutamine Supplementation Prevents Chronic Stress-Induced Mild Cognitive Impairment

• Published in: Nutrients Vol. 12; no. 4; p. 910
• Main Authors: Baek, Ji Hyeong, Jung, Soonwoong, Son, Hyeonwi, Kang, Jae Soon, Kim, Hyun Joon
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 26.03.2020; MDPI
• Subjects: Alzheimer's disease; Animal cognition; Animals; Behavior, Animal - drug effects; chronic stress; Cognitive ability; Cognitive Dysfunction - etiology; Cognitive Dysfunction - physiopathology; Corticosterone; Dementia; Disease Models, Animal; Enzymes; Glutamatergic transmission; Glutamine; Glutamine - pharmacology; Hippocampus; Hippocampus - drug effects; Immobilization; Impairment; Inflammation; Male; Maze Learning - drug effects; Memory; Mice; Mice, Inbred C57BL; mild cognitive impairment; NAD(P)H oxidase; Neurological disorders; Neuroprotective Agents - pharmacology; Neurotransmission; Nitric oxide; Nitric-oxide synthase; Oxidative stress; Oxidative Stress - drug effects; Plasma; Plasma levels; Prefrontal cortex; Stress; Stress, Psychological - complications; Stress, Psychological - physiopathology; United States > US; Austria; South Korea; Chronic stress; mild cognitive impairment; glutamine; oxidative stress
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu12040910

We recently reported that glutamine (Gln) supplementation protected glutamatergic neurotransmission from the harmful effects of chronic stress. Altered glutamatergic neurotransmission is one of the main causes of cognitive disorders. However, the cognitive enhancer function of Gln has not been clearly demonstrated thus far. Here, we evaluated whether and how Gln supplementation actually affects chronic stress-induced cognitive impairment. Using a chronic immobilization stress (CIS) mouse model, we confirmed that chronic stress induced mild cognitive impairment (MCI) and neuronal damage in the hippocampus. In contrast, Gln-supplemented mice did not show evidence of MCI. To investigate possible underlying mechanisms, we confirmed that CIS increased plasma corticosterone levels as well as brain and plasma levels of reactive oxygen/nitrogen species. CIS also increased levels of inducible nitric oxide synthase and NADPH oxidase subunits (p47 and p67 ) in both the prefrontal cortex and CA1 region of the hippocampus. CIS decreased the number of synaptic puncta in the prefrontal cortex and hippocampus, but these effects were inhibited by Gln supplementation. Taken together, the present results suggest that Gln is an effective agent against chronic stress-induced MCI.