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Absence of an insulin‐evoked Fos response in C1 neurons from diabetic rats
Author(s) -
LlewellynSmith Ida J.,
Pavia Jill M.,
Morris Margaret J.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.152
Subject(s) - endocrinology , medicine , insulin , adrenergic neurons , catecholaminergic cell groups , saline , chemistry , hypoglycemia , medulla , diabetes mellitus , streptozotocin , dopamine , adrenergic , tyrosine hydroxylase , receptor
A subset of adrenergic C1 neurons in the ventrolateral medulla help to regulate blood glucose levels by controlling hypoglycemia‐induced adrenaline secretion. Here, we characterized the response of C1 neurons to insulin‐evoked hypoglycemia in normal and diabetic rats. Five weeks after streptozotocin (STZ; 48 mg/kg i.v.) or citrate buffer (VEH) treatment, male Sprague‐Dawley rats were given either insulin (70 or 20 IU/kg, respectively) or saline and perfused at 2 hours. Medulla sections were immunostained to reveal Fos (black peroxidase reaction product) plus phenyl‐ethanolamine‐N‐methyltransferase (PNMT; brown product). Fos‐positive and ‐negative PNMT neurons in the ventral medulla were counted from the calamus scriptorius to the caudal pole of the facial nucleus. Blood glucose was five times higher in STZ than VEH rats (25.4 vs 5.2 mmol/l). In rats treated with VEH + insulin, 107.3 ± 39.2 (mean ± SD, n = 4) of the 317.0 ± 40.8 PNMT neurons (about 35%) were Fos‐positive. In rats treated with STZ + insulin, only 9.0 ± 1.0 (n = 4) of the 295.8 ± 22.6 PNMT neurons (about 1%) were Fos‐positive. A similar number of PNMT neurons were Fos‐positive in rats treated with STZ + saline or VEH + saline. These results show that diabetes profoundly depresses Fos expression in hindbrain neurons controlling adrenaline secretion. The physiological mechanisms underlying this substantial change in activity require investigation.