Brain Lesions in an Infant Rhesus Monkey Treated with Monosodium Glutamate

Olney, John W.; Sharpe, Lawrence G.

doi:10.1126/science.166.3903.386

Cited by 429 publications

(162 citation statements)

References 6 publications

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“…The accurate nucleus of the hypothalamus was particularly vulnerable to MSGinduced lesions in the infant mouse, rat, rabbit and a single immature rhesus monkey injected subcutaneously with doses of MSG ranging from 0.5 to 2.7 g/kg body weight (Olney and Sharpe, 1969). Table (2) concluded that in the 3 rd generation the inversion 2L(Cy) on the chromosome two which decreased from 20% (control or natural population) to 6% (2.0 g/l) and 4% (0.2 g/l), respectively of quinine (QUI), on the other hand decreased to 4% (10 g/l) and did not change throughout the higher concentration (22 g/l) of monosodium glutamate (MSG) the same result was reached for the higher concentration of MSG with other types of inversions except 3R (C) where completely disappeared (Fig.…”

Section: Resultsmentioning

confidence: 99%

GENETIC AND BEHAVIORAL INFLUENCES OF QUININE AND MONOSODIUM GLUTAMATE ON Drosophila melanogaster

El-Keredy

2014

Egyptian Journal of Genetics and Cytology

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Section: Resultsmentioning

confidence: 99%

GENETIC AND BEHAVIORAL INFLUENCES OF QUININE AND MONOSODIUM GLUTAMATE ON Drosophila melanogaster

El-Keredy

2014

Egyptian Journal of Genetics and Cytology

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“…The rationale of the study was based on the premise that damage of neu rons in the penumbra of a focal ischemic infarction may result from liberation, by ischemia, of L-GlU (Olney and Sharpe, 1969;Benveniste et al, 1984;Choi, 1990). L-Glu, acting through the NMDA sub type of L-Glu receptor (Rothman and Olney, 1987;Siesjo and Bengtsson, 1989), will, by increasing in tracellular Ca2 +, activate the constitutive form of (MCA occlusion only; n = 6), rilmenidine-treated (RIL; 0.75 mg/kg; n = 4), and N-w-nitro-L-arginine-treated (NNA; 2.4 mg/kg/h for 1 h; n = 6) animals.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Nitric Oxide Synthesis Increases Focal Ischemic Infarction in Rat

Yamamoto

Golanov

Berger

et al. 1992

J Cereb Blood Flow Metab

230

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Summary:We investigated whether inhibition of nitric oxide (NO) biosynthesis with N-w-nitro-L-arginine (NNA), a competitive inhibitor of NO synthase (NOS), would modify the volume of the focal ischemic infarction produced by occlusion of the middle cerebral artery (MCA) in spontaneously hypertensive rats. NNA was in fused for 1 h (2.4 mg/kg/h) immediately following occlu sion of the MCA. NNA increased lesion volume 24 h later by 32% over controls (150.8 ± 16.6 to 199.2 ± 17.4 mm3; p < 0.001, n = 6). This effect was antagonized by co infusion of L-but not D-arginine. The antihypertensive rilmenidine (0.75 mg/kg) reduced the lesion by 27% (p < 0.05, n = 4). Changes in lesion size were confined to the penumbra. NNA increased arterial pressure (AP) (118 ± There is increasing evidence that the endogenous vasodilator nitric oxide (NO) is synthesized in the brain from the amino acid L-arginine (L-Arg) by the enzyme NO synthase (NOS). The principal form of NOS expressed in brain appears to correspond to the constitutive form of the enzyme (Bredt and Sny der, 1990; Hope et ai., 1991)

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“…In 1969, Olney and Sharpe reported on brain lesions, obesity, and other disturbances in mice (Olney, 1969), and in an infant rhesus monkey (Olney and Sharpe, 1969) Obesity, voracity, and short stature M Hermanussen et al damage hitherto described, are voracity, and impaired GH secretion. However, all of these studies focussed on parenterally administered MSG.…”

Section: Discussionmentioning

confidence: 99%

Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite

Hermanussen¹,

García

Sunder³

et al. 2005

Eur J Clin Nutr

108

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Background: World-wide obesity has risen to alarming levels. We present experimental support for a new and very challenging hypothesis linking obesity, voracity, and growth hormone (GH) deficiency, to the consumption of elevated amounts of the amino-acid glutamate (GLU). Supraphysiological doses of GLU are toxic for neuronal cells. Methods: Human data were obtained from 807 592 German conscripts born between 1974 and 1978, and from 1 432 368 women of the German birth statistics (deutsche Perinatalerhebung) 1995-1997. The effects of orally administered monosodium glutamate (MSG) were investigated in 30 pregnant Wistar rats and their offspring. Pregnant animals either received no extra MSG, or 2.5 g MSG, or 5 g MSG per day, up to the end of the weaning period. In all, 2.5 g, respectively 5 g, MSG accounted for some 10%, respectively 20%, of dry weight of the average daily food ration. After weaning, MSG feeding was continued in the offspring. Findings: Morbid obesity associates with short stature. Average stature of conscripts progressively declines when body mass index increases above 38 kg/m 2 . Also morbidly obese young women are shorter than average though to a lesser extent than conscripts. Oral administration of MSG to pregnant rats affects birth weight of the offspring. Maternal feeding with 5 g MSG per day results in severe birth weight reduction (Po0.01). Weight increments remain subnormal when MSG feeding to the mothers is maintained during weaning (Po0.01). GH serum levels are affected in animals that received MSG during prenatal life via maternal feeding. Animals that are kept on high MSG diet (5 g MSG per day) continue to show serum GH levels that are as low or even lower than those of MSG injected animals (Po0.05), both at day 30 and at day 90 of life. Animals that were kept on medium MSG diet (2.5 g MSG per day) showed low serum GH levels at day 30 of life (Po0.01), but seemed to partially recover before day 90. Almost identical results were observed in IGF-1 serum levels. Oral MSG resulted in dose dependent voracity. The animals fed 5 g MSG per day increased water uptake by threefold (Po0.01), and food uptake by almost two-fold (Po0.01). The influence of MSG is in general more marked in males than in females. Interpretation: GLU is a widely used nutritional substance that potentially exhibits significant neuronal toxicity. Voracity, and impaired GH secretion are the two major characteristics of parenterally administered GLU-induced neuronal damage. GLU maintains its toxicity in animals even when administered orally. Males appear to be more sensitive than females. The present study for the first time demonstrates, that a widely used nutritional monosubstance -the flavouring agent MSG -at concentrations that only slightly surpass those found in everyday human food, exhibits significant potential for damaging the hypothalamic regulation of appetite, and thereby determines the propensity of world-wide obesity. We suggest to reconsider the recommended daily allowances of amino acids and nutritional prot...

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Brain Lesions in an Infant Rhesus Monkey Treated with Monosodium Glutamate

Cited by 429 publications

References 6 publications

GENETIC AND BEHAVIORAL INFLUENCES OF QUININE AND MONOSODIUM GLUTAMATE ON Drosophila melanogaster

GENETIC AND BEHAVIORAL INFLUENCES OF QUININE AND MONOSODIUM GLUTAMATE ON Drosophila melanogaster

Inhibition of Nitric Oxide Synthesis Increases Focal Ischemic Infarction in Rat

Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite

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