Premium
Alterations in β‐adrenergic receptors in frontal cortex and amygdala in rats with heart failure: Effects of chronic antidepressant treatment
Author(s) -
Lundberg Peter,
Henze Marcus,
Glasgow Jaimee,
Battaglia George,
Scrogin Karie
Publication year - 2009
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.23.1_supplement.938.4
Subject(s) - medicine , endocrinology , receptor , antidepressant , serotonin , stimulation , iodocyanopindolol , adrenergic , amygdala , adrenergic receptor , hippocampus , agonist , intrinsic activity
Chronic treatment with the serotonin reuptake inhibitor, fluoxetine (FLX), decreases cardiac sensitivity to β‐adrenergic receptor stimulation in rats with congestive heart failure (CHF). To determine if β‐adrenergic receptors are altered in brain regions important in anxiety, frontal cortex and amygdale were dissected and β‐adrenergic receptors were determined at a single concentration of 0.2 nM 125 Iodocyanopindolol in 4 groups of rats (CHF‐vehicle, n=8‐9; CHF‐FLX, n=6‐8; Sham‐Vehicle, n=5; Sham‐FLX, n=6) in the absence and presence of propranolol (100 µM) to determine specific binding. 10 µM serotonin was included to preclude binding of 5‐HT receptors. β‐adrenergic receptors in the frontal cortex were significantly decreased in rats with CHF (19.3%, P<0.05) while FLX had no effect. In contrast, β‐adrenergic receptors were increased in the amygdala of rats with CHF (27.3%, P<0.05), while FLX caused an overall reduction in binding (13.2%, P<0.05). Thus, alterations in β‐adrenergic receptor binding develop in brain regions involved in behavioral and autonomic responses to stress during CHF and chronic antidepressant treatment. Supported by Loyola University.