Action of gold thioglucose on pericapillary structures in the ventromedial hypothalamus.
The administration of GTG to mice leads to death of all structures in a circumscribed area of the VMH as a result of loss of blood circulation. The loss of circulation is due to damage by GTG of neural processes adjacent to some of the capillaries in this area; damage to these processes leads to abnormal capillary permeability. Pericapillary damage occurs under conditions where capillary damage and consequent necrosis are prevented. Abnormal capillary permeability appears to follow release of a vasoactive substance from the damaged neural processes. Damage to the pericapillary neural processes by GTG is insulin-dependent and is counteracted by glucocorticoids.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D006051:Aurothioglucose / Q000494:pharmacology*; D001812:Blood-Brain Barrier / Q000187:drug effects; D001929:Brain Edema / Q000473:pathology / Q000517:prevention & control; D004305:Dose-Response Relationship, Drug; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D006046:Gold / Q000494:pharmacology*; D007031:Hypothalamus / Q000187:drug effects*; D007033:Hypothalamus, Middle / Q000187:drug effects* / Q000648:ultrastructure; D007328:Insulin / Q000494:pharmacology; D051379:Mice; D009336:Necrosis; D009474:Neurons / Q000187:drug effects
D005938:Glucocorticoids; D007328:Insulin; D006051:Aurothioglucose; D006046:Gold; D001241:Aspirin