Thyroid hormone defficiency impairs myelin compaction

THYROID HORMONE DEFFICIENCY IMPAIRS MYELIN COMPACTION^*

ANDRÉA A. FERREIRA¹, MARTA S. DE FREITAS¹, NEIDE L. DE AZEVEDO², MÁRIO J.S. PEREIRA³, JOSÉ C. NAZÁRIO¹AND PENHA C. BARRADAS¹

¹

²Departamento de Histologia e Embriologia

³Departamento de Anatomia

Instituto de Biologia Roberto Alcântara Gomes, Universidade Estadual do Rio de Janeiro, 20551-030 Rio de Janeiro, RJ, Brazil

Presented by LENY A. CAVALCANTE

We have shown that myelinated nerve fibers from hypothyroid rats display a continuous pattern of immunostaining as revealed by a monoclonal antibody against 2'3'cyclic nucleotide 3'phosphodiesterase (anti-CNPase). This finding contrasts with the pattern shown by the normal animal, suggesting a possible role for thyroid hormones on myelin compaction. To study the effects of thyroid hormone deficiency during CNS myelinogenesis, we used two approaches: 1. The sequence of expression of myelin basic protein (MBP) and myelin-associated/oligodendrocytic basic protein (MOBP) as detected by immunoblotting in the cerebellum (Cb) and corpus callosum (cc) of postnatal normal (C) and hypothyroid (H) animals from 10 to 60 days (P10 to P60); 2. The morphology of myelinated fibers as observed by electron microscopy in cc from C and H groups at P60 and P90. We evaluated the frequency of morphological abnormalities (multiple inner and outer loops and redundant myelin) and performed a morphometric analysis of myelin sheath thickness (ShT) and cytoplasmic loop thickness (CL). The onset of expression of both MOBP isoforms occurred at P25 and P30 in cc and Cb, respectively, in the C group. However, all the MOPB isoforms were weakly detectable in both regions from the H group at P30 and the higher molecular weight isoform remained reduced in cc as late as P60. The expression of MBP proteins was also delayed in the H group, but showed a recovery in both structures at P45. The morphometric analysis of the axons did not show significant differences in ShT and CL in either age. Furthermore, the frequency of multiple inner loops was higher in the H group at P60, with no significant differences at P90. Our findings suggest that 1. Hypothyroidism affects the developmental pattern of late oligodendrocytic/myelin markers and selectively impairs MOBP protein expression; 2. The thyroid hormone may modulate axo-oligodendroglial relationships as indicated by the higher frequency of multiple inner loops and the apparent decrease of compact lamellae in H group. Taken together, these data reinforce the hypothesis of a role for thyroid hormone on myelin compaction. — ( June 27, 2000 ) .

Publication Dates

• Publication in this collection
  05 Oct 2000
• Date of issue
  Sept 2000