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1 Department of Psychology, University of Washington, Seattle 98195-1525; 2 Department of Veterans Affairs, Puget Sound Health Care System, Seattle 98108; and 3 Geriatric Research, Education and Clinical Center, Veterans Affairs Puget Sound Health Care System and Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington 98195-1525
The mechanism(s)
underlying hypoglycemia-associated autonomic failure (HAAF) are
unknown. To test the hypothesis that the activation of brain regions
involved in the counterregulatory response to hypoglycemia is blunted
with HAAF, rats were studied in a 2-day protocol. Neuroendocrine
responses and brain activation (c-Fos immunoreactivity) were measured
during day 2 insulin-induced hypoglycemia (0.5 U
insulin · 100 g body
wt
1 · h1 iv for 2 h) after
day 1 hypoglycemia (Hypo-Hypo) or vehicle. Hypo-Hypo animals
demonstrated HAAF with blunted epinephrine, glucagon, and
corticosterone (Cort) responses and decreased activation of the medial
hypothalamus [the paraventricular (PVN), dorsomedial (DMH), and
arcuate (Arc) nuclei]. To evaluate whether increases in day
1 Cort were responsible for the decreased hypothalamic activation,
Cort was infused intracerebroventricularly (72 µg) on
day 1 and the response to day 2 hypoglycemia was
measured. Intracerebroventricular Cort infusion failed to alter the
neuroendocrine response to day 2 hypoglycemia, despite
elevating both central nervous system and peripheral Cort levels.
However, day 1 Cort blunted responses in two of the same
hypothalamic regions as Hypo-Hypo (the DMH and Arc) but not in the PVN.
These results suggest that decreased activation of the PVN may be
important in the development of HAAF and that antecedent exposure to
elevated levels of Cort is not always sufficient to produce HAAF.
paraventricular nucleus; stress; c-Fos; hypoglycemia-associated autonomic failure
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