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ACCUMULATION OF GLUTAMIC ACID IN THE ARCUATE NUCLEUS OF THE HYPOTHALAMUS OF THE INFANT MOUSE FOLLOWING SUBCUTANEOUS ADMINISTRATION OF MONOSODIUM GLUTAMATE 1
Author(s) -
Perez V. J.,
Olney J. W.
Publication year - 1972
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1972.tb06222.x
Subject(s) - monosodium glutamate , glutamate receptor , arcuate nucleus , hypothalamus , endocrinology , medicine , glutamic acid , chemistry , subcutaneous injection , stimulation , biology , biochemistry , amino acid , receptor
—Monosodium l ‐glutamate was injected subcutaneously into 4‐day‐old mice at a dose of 2 mg/g body wt. The infants were killed at sequential intervals after injection, the brains were frozen, and samples of the arcuate nucleus (NA), ventromedial hypothalamus (VMH) and lateral thalamus (LT) were micro‐dissected from lyophilized sections for glutamate assay. Blood glutamate levels were also determined for comparison with brain levels of glutamate at corresponding post‐injection intervals. Glutamate levels in the NA steadily increased to reach a peak value of 110.9 mmol/kg dry wt. at 3 h following injection, whereas the highest levels reached in the VMH or LT were about 41.7 mmol/kg dry wt. Return to control values of about 25 mmol/kg dry wt. occurred gradually over a period of 12–15 h in all three brain regions. Blood glutamate concentrations peaked rapidly, reaching a maximum of 40 m m within 15 min but returned precipitously to near‐baseline values (below 1 m m ) in the 1–3 h interval after injection. We discuss possible mechanisms to account for the transient marked accumulation of subcutaneously administered glutamate in the NA and how this might relate to the selective destruction of arcuate neurons which occurs simultaneously.