Abstract
The potential central neural substrate for the sympathoexcitatory effect of insulin was investigated in conscious rats using Fos expression as an index of neural activity. Fos immunoreactivity in the hypothalamus and brainstem was compared in rats infused with intracerebroventricular (i.c.v.) insulin or saline for 60 min. The insulin had no effect on Fos expression in any brain nuclei. Likewise, a 90-min intravenous infusion of insulin (euglycemic) had no effect on brain Fos immunoreactivity. However, when blood glucose was allowed to decrease, Fos expression did increase in the arcuate nucleus and in the brainstem. These data do not provide any evidence to support the idea that insulin can act within the central nervous system to increase sympathetic nervous outflow.
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