Monosodium glutamate induced lesions of the arcuate nucleus. II. Fluorescence histochemistry of catecholamines

Abstract

The effect of the monosodium glutamate (MSG) induced lesion of the arcuate nucleus on catecholamines in the arcuate nucleus and median eminence of the mouse hypothalamus was determined using the Falck-Hillarp histofluorescence technique. The number of fluorescent perikarya in the arcuate nucleus of treated animals was decreased approximately 60%; the fluorescence intensity of surviving neurons was notably reduced. These changes were accompanied by a reduction in the intensity of fluorescence in the median eminence. Pretreatment of control and MSG-lesioned animals with a monoamine oxidase inhibitor (pargyline) greatly increased fluroescence in the median eminence and arcuate nucleus of both groups. However, the number of fluorescing perikarya of the arcuate nucleus of the normal pargyline treated group far exceeded that of the pargyline MSG animals. It is concluded that neonatally administered MSG caused destruction of a large number of dopaminergic arcuate perikarya.

Impact of transient correction of increased adrenocortical activity in hypothalamo-damaged, hyperadipose female rats

“…Monosodium L-glutamate (MSG) administration in neonatal rats is recognized to mainly damage hypothalamic arcuate nucleus (ARC) neurons. [1][2][3] MSG-induced partial hypothalamic denervation alters several neuroendocrine-metabolic functions. It has been proposed that early loss of hypothalamic neurotransmitters induced by MSG, namely in the ARC, 1,4,5 is responsible for such abnormalities.…”

“…Among these, MSG animals develop a number of morphological, behavioral, and endocrine abnormalities. 2,3,4,6,7 Also, the changes in hypothalamic neuronal function particularly enhance hypothalamo-pituitary-adrenal (HPA) axis activity. [8][9][10][11][12] It is known that hypophagic, 13 MSG-damaged rats are characterized by increased adiposity and insulin resistance; 14 however, the exact mechanisms whereby these abnormalities develop are not fully understood.…”

Decreased lipolysis and enhanced glycerol and glucose utilization by adipose tissue prior to development of obesity in monosodium glutamate (MSG) treated-rats

“…Neonatal administration of monosodium glutamate (MSG) to rodents destroys 80 ± 90% of the arcuate nuclei neurons 1,2 and injures other central structures 3 resulting in several neuroendocrine and metabolic abnormalities, including arrested growth and obesity. 3,4 Unlike obesity induced by gold thioglucose or bipiperidyl mustard which are associated with hyperphagia, obesity in neonatal MSG-treated rodents, is not a result of overeating. In mice, MSG obesity is associated with a doubling of metabolic ef®ciency, 5 secondary to the high level of corticosterone.…”

Insulin Secretion and Acetylcholinesterase Activity in Monosodium <i>L</i>-Glutamate-Induced Obese Mice

“…When applied to neonatal rats and mice, high levels of amino acid excitotoxic glutamate destroy hypothalamic areas, such as arcuate nuclei and median eminence [1, 2, 3]. Treatment with monosodium L -glutamate (MSG) causes obesity without any increase of food intake [4, 5].…”