Gold thioglucose selectively damages dorsal vagal nuclei.
To characterize the lesion produced in the medulla oblongata by gold thioglucose (GTG), the present experiment quantified the medullary damage in C57B1 mice that had become obese after treatment with 800 mg/kg of GTG at 30 days of age. At the rostrocaudal level of the area postrema, the neurotoxin destroyed up to 75% of the neurons in the medial cell column of the dorsal motor nucleus of the vagus (DMX), while sparing the lateral pole of the nucleus. GTG also produced significant tissue loss in the central and commissural subnuclei of the nucleus of the solitary tract (NST). In contrast, the GTG lesion did not affect cell number in the hypoglossal nucleus or reduce the volume of the area postrema. Additional observations indicated that at 48-72 h after GTG administration the affected regions of the medulla already show advanced necrosis including cell loss and gliosis; and when the relative contributions of hypothalamic, DMX, and NST damage to the obesity that develops are evaluated statistically with partial correlational analysis, it appears the the obesity primarily correlates with the hypothalamic lesion produced by GTG.
Powley
T L
TL
Prechtl
J C
JC
D000818:Animals; D006051:Aurothioglucose / Q000633:toxicity*; D001927:Brain Diseases / Q000139:chemically induced; D002452:Cell Count; D005260:Female; D005911:Gliosis; D006046:Gold / Q000633:toxicity*; D008526:Medulla Oblongata / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D014630:Vagus Nerve / Q000473:pathology
D006051:Aurothioglucose; D006046:Gold