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N. Lemkey-Johnston, W. A. Reynolds, Nature and Extent of Brain Lesions in Mice Related to Ingestion of Monosodium Glutamate: A Light and Electron Microscope Study, Journal of Neuropathology & Experimental Neurology, Volume 33, Issue 1, January 1974, Pages 74–97, https://doi.org/10.1097/00005072-197401000-00006
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Abstract
The incidence of arcuate neuron damage following 1 to 4 mg/gm oral doses of monosdoium glutamate (MSG) to neonatal mice was studied. The first morphological manifestation of the lesion involved edematous astrocytic glia and pathological changes in neurons close to the median eminence within 15–20 minutes. The sequence of the lesion involved at least three phases: 1) neuronal edema and death, 2) multiple phagocytic cells, viz. a type of “dense” cell and an electron “lucid” cell astrocyte, and 3) proliferation of astrocytic processes. It was noted that at 4 mg doses, the lesions occurred in other areas such as tectum, habenular nuclei, subfornical organ, dorsolateral surface of the thalamus, dentate-hippocampal gyri, cerebral cortex, and in the lower medulla, the nuclei gracilis and cuneatus and area postrema. In all. these structures, the lesion was initiated superficially and radiated inward, suggesting an inflow of the deleterious agent from the cerebrospinal fluid. Comparison of our neuropathological findings with those of others, emphasized the critical aspects of species variation, developmental age, route of administration, time of examination of brain material after dosage and thoroughness of sampling methods.
- edema
- cerebral cortex
- astrocytes
- cell nucleus
- drug administration routes
- glutamates
- habenula
- hippocampus
- newborn
- median eminence of hypothalamus
- neuroglia
- neurons
- sodium glutamate
- subfornical organ
- thalamus
- brain
- cerebrospinal fluid
- mice
- area postrema
- brain lesions
- ingestion
- glutamate
- microscopes
- gracilis muscle
- developmental age