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 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. Infusion of several other amino acids also damaged neurons while sparing axons of passage.
D000596:Amino Acids / Q000494:pharmacology*; D000818:Animals; D001369:Axons / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D005247:Feeding Behavior / Q000187:drug effects*; D005260:Female; D005971:Glutamates / Q000494:pharmacology*; D007031:Hypothalamus / Q000187:drug effects* / Q000473:pathology; D051381:Rats; D012970:Sodium Glutamate / Q000494:pharmacology*
D000596:Amino Acids; D005971:Glutamates; D012970:Sodium Glutamate