Changes in hippocampal synaptic functions and protein expression in monosodium glutamate‐treated obese mice during development of glucose intolerance

Abstract

Glucose is the sole neural fuel for the brain and is essential for cognitive function. Abnormalities in glucose tolerance may be associated with impairments in cognitive function. Experimental obese model mice can be generated by an intraperitoneal injection of monosodium glutamate (MSG; 2 mg/g) once a day for 5 days from 1 day after birth. MSG-treated mice have been shown to develop glucose intolerance and exhibit chronic neuroendocrine dysfunction associated with marked cognitive malfunctions at 28-29 weeks old. Although hippocampal synaptic plasticity is impaired in MSG-treated mice, changes in synaptic transmission remain unknown. Here, we investigated whether glucose intolerance influenced cognitive function, synaptic properties and protein expression in the hippocampus. We demonstrated that MSG-treated mice developed glucose intolerance due to an impairment in the effectiveness of insulin actions, and showed cognitive impairments in the Y-maze test. Moreover, long-term potentiation (LTP) at Schaffer collateral-CA1 pyramidal synapses in hippocampal slices was impaired, and the relationship between the slope of extracellular field excitatory postsynaptic potential and stimulus intensity of synaptic transmission was weaker in MSG-treated mice. The protein levels of vesicular glutamate transporter 1 and GluA1 glutamate receptor subunits decreased in the CA1 region of MSG-treated mice. These results suggest that deficits in glutamatergic presynapses as well as postsynapses lead to impaired synaptic plasticity in MSG-treated mice during the development of glucose intolerance, though it remains unknown whether impaired LTP is due to altered inhibitory transmission. It may be important to examine changes in glucose tolerance in order to prevent cognitive malfunctions associated with diabetes.

Endocrine disruptors also function as nervous disruptors and can be renamed endocrine and nervous disruptors (ENDs)

“… 116 Monosodium glutamate Food Additive Foran et al [ 310 ]: Auditory hindbrain atrophy and anomalous calcium binding protein expression after neonatal exposure. Sadek et al [ 311 ]: induced neurotoxicity by cholinergic dysfunction, Bcl-2/Bax balance, and antioxidant enzymes gene transcripts in rats Sasaki-Hamada et al [ 312 ]: Changes in hippocampal synaptic functions and protein expression in obese mice. Lau et al [ 313 ]: glutamate excitotoxicity has also been linked to chronic neurodegenerative disorders such as amyotrophic lateral sclerosis; evidence for the product excitotoxicity in acute neurologic diseases 117 n-Butylbenzene Chemical Synthesis Chalansonnet et al [ 314 ]: a decrease in the concentrations of free malondialdehyde in brain structures was observed after acute administration of this product.…”

The Role of Glucagon-Like Peptide-1 Receptor Agonists (GLP-1 RA) in Diabetes-Related Neurodegenerative Diseases

“…Sasaki-Hamada showed that disruption of synaptic plasticity occurs in the prediabetes stage, when glucose tolerance is impaired. 129 Further, the onset age 130 and duration of diabetes mellitus 131 may have some influence on synaptic plasticity. However, short-term acute changes in glucose concentrations may not directly contribute to the synaptic plasticity associated with diabetes, unless extremely severe.…”

Use of monosodium glutamate in foods: the good, the bad, and the controversial side

“…The MSG used for the induction of weight gain in hospitalized patients showed a positive influence; however, it could also be correlated with obesity in nonhospitalized individuals. MSG applied to obese mice by injection (2 mg/g) once daily for 5 days from the first day of life showed chronic neuroendocrine dysfunction and the animals developed glucose intolerance 39 . Mondal et al 40 A study carried out with 90 pregnant rats weighing between 150±20 g determined the role of MSG in comparison to high-calorie feed.…”