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To evaluate the effect of Lactobacillus brevis G-101 on absorption of monosodium glutamate (MSG), we orally administered MSG with or without G-101 in mice and measured the maximum concentration (Cmax) and blood concentration curve (AUC) of MSG and γ- aminobutyric acid (GABA). Oral administration of G-101 (1 × 10(9) CFU/mouse) potently inhibited Cmax and AUC of MSG by 97.8% and 94.3%, respectively (p < 0.05), but increased those of GABA by 32.1% and 67.7%, respectively (p < 0.05). G-101 inhibited the absorption of MSG. These results suggest that G-101 may reduce the side effect of MSG by inhibiting the absorption of MSG.

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The sodium salt of glutamate (monosodium glutamate; MSG) imparts a savory/meaty taste to foods, and has been used as a flavoring agent for millennia. Past research on MSG/glutamate has evaluated its physiologic, metabolic and behavioral actions, and its safety. Ingested MSG has been found to be safe, and to produce no remarkable effects, except on taste. However, some recent epidemiologic and animal studies have associated MSG use with obesity and aberrations in fat metabolism. Reported effects are usually attributed to direct actions of ingested MSG in brain. As these observations conflict with past MSG research findings, a symposium was convened at the 13th International Congress on Amino Acids, Peptides and Proteins to discuss them. The principal conclusions were: (1) the proposed link between MSG intake and weight gain is likely explained by co-varying environmental factors (e.g., diet, physical activity) linked to the "nutrition transition" in developing Asian countries. (2) Controlled intervention studies adding MSG to the diet of animals and humans show no effect on body weight. (3) Hypotheses positing dietary MSG effects on body weight involve results from rodent MSG injection studies that link MSG to actions in brain not applicable to MSG ingestion studies. The fundamental reason is that glutamate is metabolically compartmentalized in the body, and generally does not passively cross biologic membranes. Hence, almost no ingested glutamate/MSG passes from gut into blood, and essentially none transits placenta from maternal to fetal circulation, or crosses the blood-brain barrier. Dietary MSG, therefore, does not gain access to brain. Overall, it appears that normal dietary MSG use is unlikely to influence energy intake, body weight or fat metabolism.

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Little is known about the molecular basis of differences in behavior among individuals. Here we report consistent novelty-seeking behavior, across different contexts, among honey bees in their tendency to scout for food sources and nest sites, and we reveal some of the molecular underpinnings of this behavior relative to foragers that do not scout. Food scouts showed extensive differences in brain gene expression relative to other foragers, including differences related to catecholamine, glutamate, and γ-aminobutyric acid signaling. Octopamine and glutamate treatments increased the likelihood of scouting, whereas dopamine antagonist treatment decreased it. These findings demonstrate intriguing similarities in human and insect novelty seeking and suggest that this trait, which presumably evolved independently in these two lineages, may be subserved by conserved molecular components.

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Injection of monosodium glutamate (40nmol/hemisphere) into the intermediate hyperstriatum ventrale of the day-old chick inhibits the formation of short-term memory for a single trial learning that discriminates between colours of beads. These experiments showed that an excess of glutamate close to learning could be damaging to memory. In the present experiments we have blocked the normal reuptake of glutamate and suggest that glutamate release plays a role in normal learning. Removal of glutamate, released from presynaptic neurones during learning, is achieved by various neuronal and astrocytic glutamate transporters. By blocking the primarily astrocytic removal of glutamate by the injection of L-aspartic acid beta-hydroxamate, we effectively increased extrasynaptic levels of glutamate and inhibited short-term memory in a similar manner to central injection of 40nmol glutamate per hemisphere. These experiments suggest that glutamate release within 2.5min of the learning experience is an important feature of short-term memory formation.

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P2X receptors function as ATP-gated cation channels. The P2X(7) receptor subtype is distinguished from other P2X family members by a very low affinity for extracellular ATP (millimolar EC50) and its ability to trigger induction of nonselective pores on repeated or prolonged stimulation. Previous studies have indicated that certain P2X(7) receptor-positive cell types, such as human blood monocytes and murine thymocytes, lack this pore-forming response. In the present study we compared pore formation in response to P2X(7) receptor activation in human blood monocytes with that in macrophages derived from these monocytes by in vitro tissue culture. ATP induced nonselective pores in macrophages but not in freshly isolated monocytes when both cell types were identically stimulated in standard NaCl-based salines. However, ion substitution studies revealed that replacement of extracellular Na+ and Cl- with K+ and nonhalide anions strongly facilitated ATP-dependent pore formation in monocytes. These ionic conditions also resulted in increased agonist affinity, such that 30-100 microM ATP was sufficient for activation of nonselective pores by P2X(7) receptors. Comparison of P2X(7) receptor expression in blood monocytes with that in macrophages indicated no differences in steady-state receptor mRNA levels but significant increases (up to 10-fold) in the amount of immunoreactive P2X(7) receptor protein at the cell surface of macrophages. Thus ability of ATP to activate nonselective pores in cells that natively express P2X(7) receptors can be modulated by receptor subunit density at the cell surface and ambient levels of extracellular Na+ and Cl-. These mechanisms may prevent adventitious P2X(7) receptor activation in monocytes until these proinflammatory leukocytes migrate to extravascular sites of tissue damage.

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Variations in plasma and erythrocyte concentrations of glutamate, glutamine, and alanine during the day were studied in 10 healthy men fed ordinary Taiwanese meals, first without and, 1 week later, with monosodium glutamate (MSG) added. MSG at a level of 15, 40, and 45 mg/kg (total, 100 mg/kg/d) was added, respectively, to the breakfast, lunch, and dinner meals. Heparinized blood samples were collected over 24 hours with 1- to 3-hour intervals. In both trials, plasma glutamate concentrations increased significantly after lunch and dinner. Although the circadian variations of plasma glutamate were small (between 32 and 53 micromol/L), the levels nevertheless varied significantly as a function of the time of day in both trials. Considering that the dietary intake of glutamate was high when MSG was added, the low plasma glutamate concentration over 24 hours indicates that glutamate is actively metabolized. On the other hand, the concentrations of erythrocyte glutamate (507 to 631 micromol/L) and glutamine (427 to 613 micromol/L) did not show a significant postprandial increase or circadian variation. Nevertheless, the concentration of plasma glutamine (539 to 657 micromol/L) varied significantly as a function of time in both trials. The plasma concentration of alanine (274 to 494 micromol/L) increased significantly after each meal and decreased significantly from 2:00 to 5:00 AM in both trials. Both plasma and erythrocyte alanine concentrations varied significantly as a function of time. These results show that the substantial amount of MSG intake had no apparent effect on the circadian variation profiles of blood glutamate, glutamine, and alanine.

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The aim of the present work was to examine in pigs the effect of a dietary supplementation with the flavor enhancer monosodium glutamate (MSG) on intestinal amino acid metabolism. For this purpose, pigs weighing 60 +/- 2 kg received a standard meal twice a day for 1 week, supplemented with either 10 g MSG per meal or, as control experiments, an isonitrogenous amount of glycine together with an equal amount of sodium in the form of NaCl, the animals being their own control in all experiments. At the end of this period, pigs received a MSG or glycine-NaCl-supplemented meal and samples of portal and arterial blood were collected for amino acid analysis in plasma. The results demonstrate after MSG supplementation rapid significant increases in glutamate concentration in the portal and arterial blood plasma after a test meal which resulted in a positive portoarterial difference. In comparison, after glycine-NaCl supplementation, glutamate concentrations were almost identical in portal and arterial plasma. Furthermore, significant increased aspartate concentration in the portal blood plasma was observed after MSG supplementation when compared with control experiments. When enterocytes were isolated at the end of the supplementation period from the jejunum and examined for their metabolic capacities towards L-glutamate and L-glutamine, it was found that metabolism did not differ according to the supplement used, with glutamate and glutamine being oxidized and transaminated at a similar level. It is concluded that the portal hyperglutamatemia observed shortly after the ingestion of a MSG- supplemented meal is likely due to the saturation of the intestinal capacity to metabolize glutamate with no measurable adaptation of the metabolic pathways controlling glutamate metabolism in enterocytes.

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[3H]quinuclidinyl benzilate ([3H]QNB) binding to muscarine acetylcholine receptors (mAchR) was measured in cerebral cortex and caudate nucleus of rats ata the ages of 7, 14, and 21 days, which had received a subconvulsive intraperitoneal dose of monosodium L-glutamate (MSG) (4 mg/g) on postnatal days 1, 3, 5 and 7. MSG treatment determined an increasse of mAchR density in cerebral cortex. This was 8, 15 and 25 per cent at day 7, 14 and 21, respectively. In cuadate nucleus, a significant increase of mAchR density was detected at day 7 (240 per cent). However, on postnatal day 14, mAchR binding in caudate nucleus of MSG-Treated rats was only 47 per cent higher, while at 21 days, no changes in mAchR binding were found. When MSG was injected to adults rats, no changes in brain mAchR density were detected. Data suggest that early administration of MSG affects the development of mAchR in cerebral cortex and caudate nucleus, whereas the adult brain cortical cholinergic transmission is not sensitive to parenterally administered MSG

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A model for the sodium-dependent accumulation of glutamate by synaptosomes has been presented which fits the data of Wheeler and his coworkers and supports their hypothesis of an electrogenic cotransporter. Since their hypothesis was based on experimental data on the operation of the cotransporter on the outer membrane, the model was expanded to predict events when the cotransporter was operating on both sides of the membrane. The model predicts that the accumulation of glutamate is sensitive to the synaptosomal sodium and emphasizes the importance of the sodium/potassium pump to maintain this value. A model which uses only an electrogenic form of the cotransporter on the external membrane and a neutral form on the inside of the membrane predicts too much or too little accumulation of glutamate at different membrane potentials. A model which uses an electrogenic cotransporter on the external membrane and a concentration-dependent sodium glutamate leak would require a significant increase in the permeability of sodium glutamate when the membrane depolarizes. Only the operation of all four mentioned mechanisms will fit experimental data at two different external sodium concentrations and over the range of membrane potentials measured experimentally.

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