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Updated: Dec 8, 2025
Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
Published on: March 11, 2020
Cognitive and hippocampal synaptic profiles in monosodium glutamate-induced obese mice
Sachie Sasaki-Hamada1, Yuki Hojyo2, Ryo Mizumoto2
1Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba 278-8510, Japan; Department of Physiology, School of Allied Health Sciences, Kitasato University, Sagamihara 252-0373, Japan.
Abstract:
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.
