Thyroid hormones states and brain development interactions
Top Cited Papers
- 30 April 2008
- journal article
- review article
- Published by Wiley in International Journal of Developmental Neuroscience
- Vol. 26 (2), 147-209
- https://doi.org/10.1016/j.ijdevneu.2007.09.011
Abstract
The action of thyroid hormones (THs) in the brain is strictly regulated, since these hormones play a crucial role in the development and physiological functioning of the central nervous system (CNS). Disorders of the thyroid gland are among the most common endocrine maladies. Therefore, the objective of this study was to identify in broad terms the interactions between thyroid hormone states or actions and brain development. THs regulate the neuronal cytoarchitecture, neuronal growth and synaptogenesis, and their receptors are widely distributed in the CNS. Any deficiency or increase of them (hypo- or hyperthyroidism) during these periods may result in an irreversible impairment, morphological and cytoarchitecture abnormalities, disorganization, maldevelopment and physical retardation. This includes abnormal neuronal proliferation, migration, decreased dendritic densities and dendritic arborizations. This drastic effect may be responsible for the loss of neurons vital functions and may lead, in turn, to the biochemical dysfunctions. This could explain the physiological and behavioral changes observed in the animals or human during thyroid dysfunction. It can be hypothesized that the sensitive to the thyroid hormones is not only remarked in the neonatal period but also prior to birth, and THs change during the development may lead to the brain damage if not corrected shortly after the birth. Thus, the hypothesis that neurodevelopmental abnormalities might be related to the thyroid hormones is plausible. Taken together, the alterations of neurotransmitters and disturbance in the GABA, adenosine and pro/antioxidant systems in CNS due to the thyroid dysfunction may retard the neurogenesis and CNS growth and the reverse is true. In general, THs disorder during early life may lead to distortions rather than synchronized shifts in the relative development of several central transmitter systems that leads to a multitude of irreversible morphological and biochemical abnormalities (pathophysiology). Thus, further studies need to be done to emphasize this concept.Keywords
This publication has 107 references indexed in Scilit:
- Short-Term Effects of Thyroid Hormones on Cytoskeletal Proteins Are Mediated by GABAergic Mechanisms in Slices of Cerebral Cortex from Young RatsCellular and Molecular Neurobiology, 2006
- Thyroid Hormone-Dependent Regulation of Tα1 α-Tubulin during Brain DevelopmentMolecular and Cellular Neuroscience, 2002
- Regulation of the L1 Cell Adhesion Molecule by Thyroid Hormone in the Developing BrainMolecular and Cellular Neuroscience, 2000
- Thyroid Oxidase (THOX2) Gene Expression in the Rat Thyroid Cell Line FRTL-5Biochemical and Biophysical Research Communications, 2000
- THE EFFECT OF METHIMAZOLE ON THE OXIDANT AND ANTIOXIDANT SYSTEM IN PATIENTS WITH HYPERTHYROIDISMPharmacological Research, 1998
- Cloning and Expression of a Brain-Derived TSH ReceptorBiochemical and Biophysical Research Communications, 1997
- Hyperthyroidism increases adenosine transport and metabolism in the rat heartMolecular and Cellular Biochemistry, 1995
- Principles of neural cell migrationCellular and Molecular Life Sciences, 1990
- Cytochemical identification of cerebral glycogen and glucose‐6‐phosphatase activity under normal and experimental conditions: I. Neurons and gliaJournal of Electron Microscopy Technique, 1986
- The developing caudate nucleus in the euthyroid and hypothyroid ratJournal of Comparative Neurology, 1977