Monosodium glutamate causes dose-dependent vasocontractions in rabbits.

PMID: 

Headache. 1990 Sep ;30(9):575-80. PMID: 2262310

Abstract Title: 

Vasospasm contributes to monosodium glutamate-induced headache.

Abstract: 

Consumption of monosodium glutamate has long been considered to precipitate headaches in susceptible patients. In this study the direct effects of glutamate and its metabolite, glutamine, on arterial contractility were examined using rings of rabbit aorta. In a high concentration glutamate caused significant concentration-dependent contractions (EC50, 10(-1)M; maximum tension, 188.4 +/- 33.3 mg wt tension/mg tissue). Agonists and antagonists for alpha-adrenergic, histaminergic, serotonergic, cholinergic, and GABA-nergic receptors as well as inhibition of prostaglandin synthesis failed to influence glutamate contractions. At high concentrations (10(-5)M) the calcium channel blocker, verapamil, inhibited the glutamate response. Glutamate and glutamine both exhibited concentration dependent relaxation of norepinephrine (NE), phenylephrine (PE), histamine, serotonin (5-HT), and prostaglandin F2 alpha (PGF2 alpha)-induced contractions. Kainic acid (10(-4)M), an agonist of one subpopulation of central glutamate receptor, potentiated glutamate-induced vasoconstriction; a higher concentration (10(-3)M) produced an irreversible inhibition of glutamate contractility. Only the central glutamate receptor antagonist, ketamine (10(-4)-10(-2)M), induced a reversible, concentration dependent inhibition of glutamate-induced contractions. Glutamate contractility was not dependent on extracellular calcium, an intact endothelium or neuronal function. These results demonstrate a direct effect of glutamate on peripheral arterial tone. Dietary consumption of large quantities of MSG may represent a serious health hazard to certain individuals with pre-existing vascular disease.

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Neonatal injections of monosodium glutamate induce damage of the retinohypothalamic tract.

PMID: 

J Comp Neurol. 1993 Dec 1 ;338(1):67-82. PMID: 8300900

Abstract Title: 

Neurotoxic effects of neonatal injections of monosodium L-glutamate (L-MSG) on the retinal ganglion cell layer of the golden hamster: anatomical and functional consequences on the circadian system.

Abstract: 

In rodents, daily injection of neurotoxic monosodium L-glutamate (MSG) during the postnatal period induces retinal lesions, optic nerve degeneration with an alteration of visual pathway and an absence of the b-wave in the electroretinogram. Despite this damage, electrophysiological responses subsist in the lateral geniculate bodies and synchronization of circadian rhythms to the light/dark cycle can still occur. Using two formal properties of the circadian system (entrainment and phase-shift by light), we assessed the functionality of retinal projections to the circadian clock in MSG-treated hamsters. Displaced amacrine and ganglion cell populations were quantified and retinal terminals in the suprachiasmatic nuclei were estimated. Animals received daily doses of glutamate during the first ten days after birth according to two protocols. The two treatments similarly destroyed 56% of the overall population of the ganglion cell layer: 30% of displaced amacrine and 89% of ganglion cells. Surviving ganglion neurons (7,500 cells) were evenly distributed across the entire retina except in one area of high cell density located in the temporoventral quadrant. Retinal projections of the"image-forming"pathway were drastically reduced in the dorsal lateral geniculate bodies, less in their ventral part. The"nonimage-forming"pathway was also affected since the volume of labeled terminals in the suprachiasmatic nuclei was reduced by one-half to one-third. Nevertheless, treated hamsters exhibited a free-running locomotor activity rhythm after several months in constant darkness, could be entrained by the light/dark cycle and phase-shifted by light pulses. These results suggest that a damaged retinohypothalamic tract can still assume the photic entrainment of the circadian clock.

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Rats exposed to monosodium glutamate early in life exhibit locomotor and learning deficits.

PMID: 

Neurosci Lett. 2000 Apr 21 ;284(1-2):57-60. PMID: 10771161

Abstract Title: 

Locomotor and learning deficits in adult rats exposed to monosodium-L-glutamate during early life.

Abstract: 

Neonatal administration of neurotoxic doses of monosodium-L-glutamate (MSG) to rats causes neuronal necrosis of the hypothalamus along with behavioral abnormalities. In the present study the behavioral effects in rats treated with subneurotoxic doses of MSG (2 mg/g, p.o., for 10 days) at the weaned stage were investigated at day 90 post-dosing. The MSG-treated rats did not show significant changes in any of the components of spontaneous locomotor activity but, after apomorphine challenge, marked decreases in the distance travelled, ambulatory and stereotypic times, and the number of stereotypic movements with an increase in the resting time were observed. Significant decrease in the active avoidance learning performance was observed in the MSG-treated rats in the learning (acquisition) phase without any changes in the extinction and relearning phases. The results indicate that exposure to MSG in early life in rats could lead to subtle behavioral aberrations in late adulthood.

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Monosodium glutamate is an unusual exacerbant of chronic idiopathic urticaria.

PMID: 

J Nutr. 2000 04 ;130(4S Suppl):1063S-6S. PMID: 10736383

Abstract Title: 

Additive-induced urticaria: experience with monosodium glutamate (MSG).

Abstract: 

In patients with chronic urticaria, the incidence of reactions to any additives, including monosodium glutamate (MSG), is unknown. Although many studies have investigated the association of additives and urticaria, most have been poorly designed. This study sought to determine the prevalence of reactions to additives, including MSG, in patients with chronic urticaria using a rigorous protocol. We studied 65 subjects (44 women, 21 men; ages 14-67). All had urticaria for>6 wk without discernible etiology. Subjects with active urticaria were studied while they were taking the lowest effective dose of antihistamine. Screening challenges to the 11 additives most commonly associated with exacerbations of chronic idiopathic urticaria were performed in a single-blind fashion. The dose of MSG given was 2500 mg. Skin scores were obtained to determine a positive reaction in an objective manner. Subjects with a positive screening challenge were rechallenged (at least 2 wk later) with a double-blind, placebo-controlled protocol as in-patients in our General Clinical Research Center. Two subjects had positive single-blind, placebo-controlled challenges, but neither had a positive double-blind, placebo-controlled challenge. We conclude, with 95% confidence, that MSG is an unusual (

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A case report of orafacial granulomatosis attributed to monosodium glutamate allergy.

PMID: 

Oral Surg Oral Med Oral Pathol. 1991 May ;71(5):560-4. PMID: 2047097

Abstract Title: 

Monosodium glutamate-related orofacial granulomatosis. Review and case report.

Abstract: 

A case is reported in a 15-year-old white girl who had a swollen lower face and lips; a diagnosis of orofacial granulomatosis was made. It was suspected that her condition had an allergic basis because an increase in clinical signs and symptoms was shown to be related to the food additive monosodium glutamate. Treatment with a restricted diet resulted in resolution of the facial swelling.

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Monosodium glutamate induces convulsions in adult rats and is potentiated by hyperthermia.

PMID: 

Amino Acids. 1991 Feb ;1(1):81-9. PMID: 24194050

Abstract Title: 

Monosodium glutamate induced convulsions in rats: Influence of route of administration, temperature and age.

Abstract: 

Treatment of developing rats with monosodium glutamate (MSG) produces an increase of glutamate levels in the brain, being this elevation dependent on both route of administration and animal's age. The capacity of exogenous MSG to induce convulsions seems to be related to the rate of glutamate elevation in the brain, rather than to the absolute value of glutamate concentration reached. Short exposure of MSG-treated rats to moderate hyperthermia potentiated the convulsive incidence and extended the brain damage to areas not affected by treatment with MSG alone, suggesting that the synergic effect of hyperthermia on glutamate neurotoxicity may be related to an increase in the permeability of the blood-brain barrier in the hyperthermic developing rats.

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Monosodium glutamate induced convulsions upon injection in adults rats.

PMID: 

Gen Pharmacol. 1985 ;16(5):489-93. PMID: 4054574

Abstract Title: 

Monosodium L-glutamate-induced convulsions–II. Changes in catecholamine concentrations in various brain areas of adult rats.

Abstract: 

Norepinephrine (NE) and dopamine (DA) levels in various brain regions were measured in a model of experimentally produced convulsions by monosodium L-glutamate (MSG) administration to adult rats. Stress by injection of all solutions produced a 60% decrease in NE level in forebrain, recovering its basal value at 15 min after injection. A significant reduction of brain NE and DA levels of MSG-injected animals was found in the preconvulsive stage, particularly in the forebrain. No significant variations in catecholamine levels were seen in brain stem and cerebellum as a result of MSG injection. It is suggested that the changes found in endogenous catecholamine concentration in the forebrain may play a physiological role in the mechanisms of production of convulsions in the MSG model.

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Prenatal monosodium glutamate treatment given through the mother’s diet causes behavioral deficits and obesity in rat offspring.

PMID: 

Int J Neurosci. 1984 Apr ;23(2):117-26. PMID: 6541212

Abstract Title: 

Prenatal monosodium glutamate (MSG) treatment given through the mother's diet causes behavioral deficits in rat offspring.

Abstract: 

The present study reports various developmental and behavioral changes in the offspring of rat dams that received monosodium glutamate (MSG) in the drinking water all through the second and third trimesters of pregnancy. Three main effects were observed in the MSG exposed offspring: (1) juvenile obesity; (2) reduced general activity levels; (3) a specific type of learning disability in discrimination learning involving choice between simultaneously present positive and negative stimuli.

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The pertussis virus used for the pertussis vaccine is grown using monosodium glutamate.

PMID: 

Appl Microbiol. 1970 Mar ;19(3):512-20. PMID: 4314842

Abstract Title: 

Use of glutamic acid to supplement fluid medium for cultivation of Bordetella pertussis.

Abstract: 

The amino acid consumption by Bordetella pertussis growing in broth containing casein hydrolysate was examined. Serine, proline, alanine, glycine, aspartate, and glutamate were rapidly consumed, in a manner which suggested that they supplied the energy requirements of the organism; exhaustion of the energy source appeared to be the main factor limiting the yield of cells. There was no correlation between the utilization of individual amino acids and the phase of growth; uptake appeared to depend only upon relative concentrations. Consumption of threonine, phenylalanine, histidine, leucine, and methionine was slight; consumption of valine and lysine was variable, and isoleucine was excreted. The addition of monosodium l-glutamate (3 mg/ml) to the broth in shaken flasks increased the cell yield by an average of 43.5%. It had no detectable adverse effect upon the agglutin-producing capacity, agglutinability in antisera versus smooth and rough growth phases, mouse-lethal toxicity, histamine-sensitizing factor potency, or intracerebral protective potency of the culture. Broth supplemented with monosodium l-glutamate has been used over a 2-year period to prepare experimental vaccines by both batch and continuous cultivation methods at controlled pH; the cell yields obtained from the supplemented broth have been up to 52% higher than those from the basal broth. The use of glutamate to replace a proportion of casein hydrolysate in the broth caused a reduction in the cell yield, an alteration in cell morphology, and reduction in the mouse-lethal toxicity, the histamine-sensitizing factor potency, and the intracerebral protective potency of the cells.

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