Abstract

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 (p47phox and p67phox) 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.

Highlights

  • Mild cognitive impairment (MCI) represents a mental stage between normal aging and dementia.It involves problems with memory, language, clarity of thinking, and judgment, without interfering with daily life and common activities [1]

  • Gln has been reported to be neuroprotective against oxidative stress and inflammation [17]. These results suggest that Gln might protect the brain from chronic stress-induced MCI

  • There was no significant difference in motor activity between groups (Figure 2)

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Summary

Introduction

Mild cognitive impairment (MCI) represents a mental stage between normal aging and dementia. It involves problems with memory, language, clarity of thinking, and judgment, without interfering with daily life and common activities [1]. MCI has been reported to increase the risk of developing dementia caused by Alzheimer’s disease (AD) and other neurological disorders [1,2]. Emerging evidence has shown that disturbed glutamatergic neurotransmission in the central nervous system is one of the main causes of emotional and cognitive disorders [3,4,5,6]. We recently reported that reduced glutamine synthetase activity during synaptogenesis resulted in a spatial memory impairment in adult mice and in reductions in both synaptic puncta and glutamatergic neurotransmission in the hippocampus [10]

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