Cognitive and hippocampal synaptic profiles in monosodium glutamate-induced obese mice
Autor: | Sachie Sasaki-Hamada, Shoko Yanagisawa, Ryo Mizumoto, Yuki Hojyo, Jun-Ichiro Oka, Hajime Koyama |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Monosodium glutamate Long-Term Potentiation Hippocampus Mice Obese Hippocampal formation Synaptic Transmission 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Cognition Postsynaptic potential Internal medicine Sodium Glutamate medicine Animals Recognition memory Neuronal Plasticity business.industry General Neuroscience Long-term potentiation General Medicine 030104 developmental biology Endocrinology nervous system chemistry Synapses Facilitation business 030217 neurology & neurosurgery |
Zdroj: | Neuroscience research. 170 |
ISSN: | 1872-8111 |
Popis: | 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. |
Databáze: | OpenAIRE |
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