Retinoic acid reverses the PTU related decrease in neurogranin level in mice brain.

V. Enderlin, J. Vallortigara, S. Alfos, C. Féart, V. Pallet, P. Higueret
J. Physiol. Biochem.. 2004-09-01; 60(3): 191-198
DOI: 10.1007/bf03167028

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1. J Physiol Biochem. 2004 Sep;60(3):191-8.

Retinoic acid reverses the PTU related decrease in neurogranin level in mice

Enderlin V(1), Vallortigara J, Alfos S, Féart C, Pallet V, Higueret P.

Author information:
(1)Unité de Nutrition et Signalisation Cellulaire (E.A. MENRT; USC INRA) ISTAB,
Université Bordeaux 1, Avenue des Facultés, 33405 Talence cedex, France.

Recent data have shown that fine regulation of retinoid mediated gene expression
is fundamentally important for optimal brain functioning in aged mice.
Nevertheless, alteration of the thyroid hormone signalling pathway may be a
limiting factor, which impedes retinoic acid (RA) from exerting its modulating
effect. Mild hypothyroidism is often described in the elderly. Thus, in the
present study, it was of interest to determine if RA exerts its neurological
modulating effect in mild hypothyroidism. To obtain further insight into this
question, mice were submitted to a low propylthiouracyl (PTU) drink (0.05%) in
order to slightly reduce the serum level of triiodothyronine (T3). A quantitative
evaluation of RA nuclear receptors (RAR, RXR), T3 nuclear receptor (TR) and of
neurogranin (RC3, a RA target gene which codes for a protein considered as a good
marker of synaptic plasticity) in PTU treated mice injected with vehicle or RA or
T3 was carried out. The PTU-related decrease in expression of RAR, RXR and RC3
was restored following RA or T3 administration, as observed in aged mice. The
amount of TR mRNA, which was not affected in PTU treated mice, was increased only
after T3 treatment as observed in overt hypothyroidism. These results suggest
that neurobiological alterations observed in aged mice are probably related to RA
and T3 signalling pathway modifications associated, in part, with mild changes in
thyroid function.

DOI: 10.1007/BF03167028
PMID: 15700765 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus