A glial toxin reduces effects of gold thioglucose on the hypothalamus and area postrema.
To see if DL-alpha amino adipate (DL-AA) an agent known to cause transient swelling and dysfunction of hypothalamic glia, would affect the ability of goldthioglucose (GTG) to cause hypothalamic lesions, groups of male, 100 g rats were given saline, 0.5 mg/g of DL-AA, or 0.75 mg/g of DL-AA 30 min before injection of 0.4 mg/g of GTG. The incidence of GTG lesions was significantly less in the DL-AA treated groups than in the saline treated group. Histochemical staining of brain tissue revealed the existence of a population of specialized iron-containing glia with an anatomical distribution similar to the specific areas in the hypothalamus area postrema most sensitive to GTG. The results suggest that GTG lesion formation may result from an effect of GTG on glia.
D015074:2-Aminoadipic Acid / Q000494:pharmacology*; D000600:Amino Acids, Dicarboxylic / Q000494:pharmacology*; D000818:Animals; D006051:Aurothioglucose / Q000037:antagonists & inhibitors / Q000633:toxicity*; D001786:Blood Glucose / Q000032:analysis; D002552:Cerebral Ventricles / Q000187:drug effects* / Q000473:pathology; D006046:Gold / Q000633:toxicity*; D007031:Hypothalamus / Q000187:drug effects* / Q000473:pathology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D000600:Amino Acids, Dicarboxylic; D001786:Blood Glucose; D015074:2-Aminoadipic Acid; D006051:Aurothioglucose; D006046:Gold