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Thyroid hormone regulates oxidative phosphorylation in the cerebral cortex and striatum of neonatal rats
Author(s) -
Martinez Bienvenida,
Del Hoyo Pilar,
Martin Miguel Angel,
Arenas Joaquín,
PerezCastillo Ana
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00487.x
Subject(s) - striatum , endocrinology , medicine , oxidative phosphorylation , cerebral cortex , hippocampus , thyroid , mitochondrion , biology , thalamus , cortex (anatomy) , cerebellum , central nervous system , hormone , chemistry , neuroscience , biochemistry , dopamine
We have previously shown that thyroid hormone (T 3 ) regulates mitochondrial gene expression, morphology and transmembrane potential in the developing brain. Here, we have analysed the effect of thyroid hormone on mitochondrial function in different brain regions. For this purpose we have determined, in control, hypothyroid and T 3 ‐treated hypothyroid neonatal rats, the rate of oxidative phosphorylation in isolated mitochondria and the activity of the respiratory complexes in tissue homogenates. Our results showed a decrease in oxidative phosphorylation rate (only in the presence of NADH‐generating substrates) and mitochondrial complexes I and III activity in the cerebral cortex and striatum of hypothyroid neonates, but not in the other areas analysed (hippocampus, cerebellum, thalamus, mid brain and brain stem). In parallel with mitochondrial activity, the levels of mitochondrially encoded transcripts were decreased only in the cerebral cortex and striatum of hypothyroid rats. The administration of T 3 corrected all these parameters. In summary, this study showed a down‐regulation of mitochondrial gene expression accompanied by a decrease in mitochondrial activity in the cerebral cortex and striatum of developing hypothyroid neonatal rats.