Cognitive and hippocampal synaptic profiles in monosodium glutamate-induced obese mice.

Sachie Sasaki-Hamada, Yuki Hojyo, Ryo Mizumoto, Hajime Koyama, Shoko Yanagisawa, Jun-Ichiro Oka

Neuroscience research 2021 Sep

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Obesity is a growing worldwide public health issue and is associated with a range of comorbidities, including cognitive deficits. The present study investigated synaptic changes in the hippocampus during the development of obesity. The treatment of newborn mice with monosodium-L-glutamate (MSG, 2 mg/g) induced obesity and recognition memory deficits in the novel object recognition (NOR) test at 16-17 weeks, but not at 8-9 weeks. Hippocampal synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD), and excitatory synaptic transmission at Schaffer collateral-CA1 (SC-CA1) synapses were compared between MSG-treated mice and age-matched control mice. LTP and fiber volley amplitudes were enhanced in MSG-treated mice at 16-17 weeks, but not at 8-9 weeks. Furthermore, the strength of paired-pulse facilitation (PPF) changed in MSG-treated mice at 16-17 weeks, but not at 8-9 weeks. These results suggest that enhanced LTP in the SC-CA1 synapses of MSG-induced obese mice involves presynaptic rather than postsynaptic mechanisms. Copyright © 2020 Elsevier B.V. and Japan Neuroscience Society. All rights reserved.

Citation

Sachie Sasaki-Hamada, Yuki Hojyo, Ryo Mizumoto, Hajime Koyama, Shoko Yanagisawa, Jun-Ichiro Oka. Cognitive and hippocampal synaptic profiles in monosodium glutamate-induced obese mice. Neuroscience research. 2021 Sep;170:201-207