Axon-Sparing Brain Lesioning Technique: The Use of Monosodium-L-Glutamate and Other Amino Acids

Infusions of monosodium-L-glutamate into the rostral hypothalamus, believed to contain neurons mediating satiety, produced persistent hyperphagia and obesity, thus suggesting that a brain lesion had been produced. Similar infusions into the caudal hypothalamus, believed to contain unmyelinated axons...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1977-11, Vol.198 (4316), p.515-517
Main Authors: Simson, Earl L., Gold, Richard M., Standish, L. J., Pellett, Peter L.
Format: Article
Language:English
Subjects:
Amino acids
Amino Acids - pharmacology
Animals
Anterior hypothalamus
Axons
Axons - drug effects
Body Weight - drug effects
Brain
Brain damage
Feeding Behavior - drug effects
Female
Glutamates - pharmacology
Hypothalamus
Hypothalamus - drug effects
Hypothalamus - pathology
Lesions
Neuroglia
Neurons
Rats
Sodium Glutamate - pharmacology
Weight gain
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Summary:Infusions of monosodium-L-glutamate into the rostral hypothalamus, believed to contain neurons mediating satiety, produced persistent hyperphagia and obesity, thus suggesting that a brain lesion had been produced. Similar infusions into the caudal hypothalamus, believed to contain unmyelinated axons of passage that mediate satiety, failed to alter food intake or body weight. Histological examination of the affected tissue confirmed the behavioral evidence that suggests that this technique spares axons but destroys cell bodies. Infusions of several other amino acids also damaged neurons while sparing axons of passage.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.910144