Thyroid hormones in the rat amygdala as common targets for antidepressant drugs, mood stabilizers, and sleep deprivation
Pinna G, Broedel O, Eravci M, Stoltenburg-Didinger G,
Plueckhan H, Fuxius S, Meinhold H, Baumgartner A.
Department of Radiology and Nuclear Medicine,
Universitatsklinikum Benjamin-Franklin,
Free University of Berlin, Berlin, Germany.
Biol Psychiatry. 2003 Nov 15;54(10):1049-59.


BACKGROUND: There have been repeated reports of antidepressant effects of thyroid hormones. In this study, we investigated whether antidepressant treatments enhance the concentrations of thyroid hormones in rat brain. METHODS: Each of the groups of rats was treated for 14 days with one of the following: an antidepressant drug (desipramine, paroxetine, venlafaxine, or tianeptine); a mood stabilizer (lithium or carbamazepine); or 8 hours' partial sleep deprivation. Thyroid hormone concentrations were quantified in homogenates, nuclei, mitochondria, synaptosomes, myelin, and microsomes in 11 rat brain areas. RESULTS: No drug effects were seen on nuclear triiodothyronine (T(3)) concentrations in any brain area. In the amygdala, all antidepressant drugs enhanced the levels of T(3) in the myelin fraction. Triiodothyronine molecules were identified in the myelin by immunogold labeling. Quantification of the major lipid components showed a selective decrease in cholesterol in the myelin of the amygdala after desipramine treatment. Desipramine induced an increase in protein concentrations, 3,5-diiodothyronine levels, and the activity of the mitochondrial enzyme succinate dehydrogenase in the mitochondria of the amygdala. Lithium, carbamazepine, and partial sleep deprivation raised the levels of T(3) in synaptosomes of the amygdala. CONCLUSIONS: These results demonstrate that thyroid hormones in the amygdala are a common target of different antidepressant and mood-stabilizing therapies.
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