Holzwarth-McBride M A, Sladek J R, Knigge K M
Anat Rec. 1976 Oct;186(2):197-205. doi: 10.1002/ar.1091860206.
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.
运用福尔克 - 希拉尔普组织荧光技术，测定了谷氨酸钠（MSG）诱导的弓状核损伤对小鼠下丘脑弓状核和正中隆起中儿茶酚胺的影响。经处理动物的弓状核中荧光核周体数量减少了约60%；存活神经元的荧光强度显著降低。这些变化伴随着正中隆起荧光强度的降低。用单胺氧化酶抑制剂（帕吉林）对对照动物和MSG损伤动物进行预处理，极大地增加了两组动物正中隆起和弓状核的荧光。然而，正常帕吉林处理组弓状核中发荧光的核周体数量远远超过帕吉林处理的MSG动物组。得出的结论是，新生期给予MSG会导致大量多巴胺能弓状核周体被破坏。
