The sensitivity to
insulin hypoglycemic convulsions has been shown to decrease at early times (16 and 24 hr) and increase at later times (1 week) after
gold thioglucose (GTG) treatment. Systemically administered GTG is well known to produce
hyperphagia, resulting in
obesity, and cytological damage focused relatively selectively in the ventromedial hypothalamic area (VMH). Both of these effects on
insulin hypoglycemic convulsions occur before the
weight gain, but at a time when histological damage visible with
cresyl violet stain has already appeared. Both of these changes reflect a difference in the convulsive response to
hypoglycemia, rather than a differences in the degree of
hypoglycemia in response to
insulin. No functional change in the convulsive sensitivity was found at still earlier times during the latency in establishing the histological damage visible with
cresyl violet. These results suggest that GTG lesions a relatively discrete brain region involved in adjusting the functional response of the brain to
hypoglycemia, including a composite of two opposite regulatory components. The significance of such a control center in relation to energy metabolism in brain is discussed. Moreover, it has been postulated that the
glucose moiety of GTG binds to
glucoreceptors in the VMH to focus the cytoxicity of the
gold thioportion at that site. These results are also discussed in relation to this proposed mechanism for concentration and hence localization of GTG toxicity in the VMH.