Monosodium glutamate neurotoxicity, hyperosmolarity, and blood-brain barrier dysfunction.
Rats received 3H-mannitol, which marks the intactness of the blood-brain barrier, and 14C-glutamate or 14C-aspartate by intracardiac injection after oral gavage with water, monosodium glutamate, monosodium aspartate, or sodium chloride (doses equiosmolar to 4 g/kg monosodium glutamate). Thirty min later, various brain regions (e.g., cerebellum, cortex, hypothalamus, and striatum) were assayed for tritium and carbon-14. In most regions in most animals given monosodium glutamate or hypertonic saline, the level of the carbon-14 acidic amino acid tended to parallel the extent of damage incurred by the blood-brain barrier, as indicated by high levels of tritium-labelled mannitol. These data suggest that severe hyperosmolarity may be a prerequisite for monosodium glutamate to produce neurotoxic changes, and may explain why elective dietary consumption of enormous quantities of glutamate, by animals given free access to water, fails to induce brain lesions.
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D001812:Blood-Brain Barrier / Q000187:drug effects*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D005971:Glutamates / Q000378:metabolism / Q000633:toxicity*; D008353:Mannitol / Q000378:metabolism; D009994:Osmolar Concentration; D051381:Rats; D012970:Sodium Glutamate / Q000633:toxicity*
D005971:Glutamates; D001224:Aspartic Acid; D008353:Mannitol; D012970:Sodium Glutamate