T3 administration in adult hypothyroid mice modulates expression of proteins involved in striatal synaptic plasticity and improves motor behavior.
Neurobiology of Disease. 2008-09-01; 31(3): 378-385
DOI: 10.1016/j.nbd.2008.05.015
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1. Neurobiol Dis. 2008 Sep;31(3):378-85. doi: 10.1016/j.nbd.2008.05.015. Epub 2008
Jun 4.
T3 administration in adult hypothyroid mice modulates expression of proteins
involved in striatal synaptic plasticity and improves motor behavior.
Vallortigara J(1), Alfos S, Micheau J, Higueret P, Enderlin V.
Author information:
(1)Unité de Nutrition et Neurosciences, Universités Bordeaux 1-Bordeaux 2, Avenue
des Facultés, 33405 Talence Cedex, France.
Adult-onset hypothyroidism is associated with neurological changes such as
cognitive dysfunction and impaired learning, which may be related to alterations
of synaptic plasticity. We investigate the consequence of adult-onset
hypothyroidism on thyroid-mediated transcription events in striatal synaptic
plasticity, and the effect of triiodothyronine (T3) replacement. We used
hypothyroid mice, treated with propylthiouracil (PTU) and methimazole (MMI), with
or without subsequent administration of T3. We evaluated the amount of T3 nuclear
receptors (TRalpha1, TRbeta) and striatal plasticity indicators: neurogranin
(RC3), Ras homolog enriched in striatum (Rhes), Ca2+/calmodulin-dependent protein
kinase (CaMKII), and dopamine- and cAMP-regulated phosphoprotein (DARPP-32). In
addition, we assessed hypothyroid mice motor behavior as related to striatum
synaptic functions. Hypothyroid mice exhibited significantly reduced TRbeta, RC3
and Rhes expression. T3 administration reversed the expression of TRbeta, RC3,
and up-regulated CaMKII levels as well as motor behavior, and decreased DARPP-32
protein phosphorylation. We suggest that thyroid hormone modulation had a major
impact on striatal synaptic plasticity of adult mice which produced in turn motor
behavior modifications.
DOI: 10.1016/j.nbd.2008.05.015
PMID: 18585460 [Indexed for MEDLINE]