Deficits in Water Escape Performance and Alterations in Hippocampal Cholinergic Mechanisms Associated With Neonatal Monosodium Glutamate Treatment in Mice

Wong, Peter T.-H.; Neo, H; Teo, W. L.; Hong, Feng; Xue, Yangkui; Loke, Weng‐Keong

doi:10.1016/s0091-3057(96)00338-3

Cited by 20 publications

(10 citation statements)

References 33 publications

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“…Previous studies reported that MSG‐treated rodents had behavioral abnormalities, such as changes in learning deficits (Iwata et al ., ; Wong et al ., ) and activity levels (Araujo & Mayer, ; Pizzi & Barnhart, ; Nemeroff et al ., ; Nikoletseas, ; Iwata et al ., ). These studies, however, did not detect glucose intolerance in MSG‐treated rodents.…”

Section: Discussionmentioning

confidence: 99%

“…The MSG‐treated obese rodent is a model associated with glucose intolerance that may occur without the presence of type 2 DM, depending on the age at which the rodents are studied (Olney, ; Terry et al ., ; Hirata et al ., ). Moreover, the neonatal administration of MSG to rodents caused neuronal necrosis in the hypothalamus (Hirata et al ., ; de Mello et al ., ; Matysková et al ., ) along with behavioral abnormalities such as learning impairments (Iwata et al ., ; Wong et al ., ). We here determined whether learning and memory, hippocampal synaptic plasticity, and synaptic transmission were affected by glucose intolerance in MSG‐treated obese mice.…”

Section: Introductionmentioning

confidence: 97%

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

Sasaki-Hamada

Hojo

Koyama

et al. 2015

Eur J of Neuroscience

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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.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

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

Sasaki-Hamada

Hojo

Koyama

et al. 2015

Eur J of Neuroscience

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“…Short-term memory impairment as well as physical debilitations were also thought to be responsible (31,35). In some other studies, the interaction between glutamate and the cholinergic transmission have been researched and conclusions are that the inhibition of the cholinergic mechanism, brought on by MSG may be responsible for deficient learning and memory in mice (19,36). Wong (36), in the same study concluded that NMDA glutamate receptors had decreased efficiency, and the combined deficiencies in glutamate and cholinergic system could present a very convincing explanation for the disparity between MSG-treated mice and controls.…”

Section: Discussionmentioning

confidence: 99%

Elevated Plus Maze and Y-Maze Behavioral Effects of Subchronic, Oral Low Dose Monosodium Glutamate in Swiss Albino Mice

Onaolapo¹

2012

IOSJPBS

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Effects of subchronic oral low dose monosodium glutamate (MSG) on neurobehavior were assessed using the Y and Elevated plus mazes in mice. Forty adult Swiss albino mice weighing between 20-25 g were assigned into four groups A, B, C and D. Group A served as control and received normal saline, groups B, C and D received MSG dissolved in normal saline orally at 0.5, 1.0 and 1.5 mg/kg dose. MSG or vehicle was administered for a period of 14 days, following which animals were exposed to the elevated plus maze (EPM) and the Y-maze. The numbers of entries and percentage time spent in the open and closed arms after 5mins exposure to the plus maze and Y-maze spontaneous alternations over a five minute period was scored for each animal as a measure of spatial memory. Result were analysed by one way ANOVA followed by a posthoc test, results were expressed as mean ±S.E.M. Elevated plus maze performance showed a significant decrease in the number of entries and time spent in the open arm and an increase in the total number of arm entries compared to control, Y-maze task performance showed no significant improvement in the MSG groups compared to control. The study concluded that subchronic MSG at the doses administered was anxiogenic but had only a slight retardant effect on spatial working memory.

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“…Behavioral studies have also shown that exposure to excess glutamate during critical periods of brain development can produce prolonged alterations in behavior [121,122]. The treatment with glutamate during the early postnatal period in rats resulted in defects in adjusting to a new environment 21 and 60 days later, something commonly found in ASD [123].…”

Section: Effect Of Dietary Food Additive Excitotoxinsmentioning

confidence: 99%

Immune-Glutamatergic Dysfunction as a Central Mechanism of the Autism Spectrum Disorders

Blaylock

Strunecká

2009

CMC

123

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Despite the great number of observations being made concerning cellular and the molecular dysfunctions associated with autism spectrum disorders (ASD), the basic central mechanism of these disorders has not been proposed in the major scientific literature. Our review brings evidence that most heterogeneous symptoms of ASD have a common set of events closely connected with dysregulation of glutamatergic neurotransmission in the brain with enhancement of excitatory receptor function by pro-inflammatory immune cytokines as the underlying mechanism. We suggest that environmental and dietary excitotoxins, mercury, fluoride, and aluminum can exacerbate the pathological and clinical problems by worsening excitotoxicity and by microglial priming. In addition, each has effects on cell signaling that can affect neurodevelopment and neuronal function. Our hypothesis opens the door to a number of new treatment modes, including the nutritional factors that naturally reduce excitotoxicity and brain inflammation.

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Deficits in Water Escape Performance and Alterations in Hippocampal Cholinergic Mechanisms Associated With Neonatal Monosodium Glutamate Treatment in Mice

Cited by 20 publications

References 33 publications

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

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

Elevated Plus Maze and Y-Maze Behavioral Effects of Subchronic, Oral Low Dose Monosodium Glutamate in Swiss Albino Mice

Immune-Glutamatergic Dysfunction as a Central Mechanism of the Autism Spectrum Disorders

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