Thyroid hormone and retinoids affect motoneuron phenotype and reaction after axotomy in the spinal cord of adult rats

Motoneuron phenotype in the spinal cord is regulated by an intrinsic genetic program, extrinsic environmental signals and target-derived molecules. Axonal lesions trigger a phenotype switch to foster repair phenomena and axonal re-growth. We have investigated the influence of the long-term treatment...

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Published in:	Brain research 2002-01, Vol.925 (2), p.122-132
Main Authors:	Giardino, Luciana, Giuliani, Alessandro, Bettelli, Carla, Calzà, Laura
Format:	Article
Language:	eng
Subjects:	Animals Axotomy Biological and medical sciences Calcitonin Gene-Related Peptide - genetics Calcitonin Gene-Related Peptide - metabolism Choline O-Acetyltransferase - genetics Choline O-Acetyltransferase - metabolism Diterpenes Fundamental and applied biological sciences. Psychology Gene expression regulation Gene Expression Regulation - drug effects Gene Expression Regulation - physiology Hyperthyroidism - chemically induced Hyperthyroidism - metabolism Hypothyroidism - metabolism In Situ Hybridization Male Motoneuron Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration Motor Neurons - cytology Motor Neurons - drug effects Motor Neurons - metabolism Phenotype Rat Rats Rats, Sprague-Dawley Receptor, Nerve Growth Factor Receptors, Nerve Growth Factor - genetics Receptors, Nerve Growth Factor - metabolism Retinoic acid Retinyl Esters Retrograde Degeneration - drug therapy Retrograde Degeneration - pathology RNA, Messenger - metabolism Sciatic Nerve - physiology Specific Pathogen-Free Organisms Spinal Cord - cytology Spinal Cord - drug effects Spinal Cord - metabolism Thyroid hormone Thyroid Hormones - pharmacology Vertebrates: nervous system and sense organs Vitamin A - analogs & derivatives Vitamin A - pharmacology
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Summary:	Motoneuron phenotype in the spinal cord is regulated by an intrinsic genetic program, extrinsic environmental signals and target-derived molecules. Axonal lesions trigger a phenotype switch to foster repair phenomena and axonal re-growth. We have investigated the influence of the long-term treatment with thyroid hormone and all trans retinol palmitate (RA) on motoneuron phenotype and spinal cord reaction to axotomy in adult male rats. Neurochemical markers, investigated by in situ hybridization and immunocytochemistry, included choline acetyltransferase (ChAT), calcitonin gene-related peptide (CGRP) and neurotrophin low affinity receptor p75. Treatment was administered for 56 days and then mid-thigh sciatic axotomy was performed on a number of animals from each experimental groups; the rats were examined 9 days after surgery. The results indicate that: (1) Number and size of ChAT-immunoreactive neurons in the lumbar tract of the spinal cord was reduced in hypothyroid compared to control rats, whereas steady-state level of ChAT mRNA in labelled motoneurons failed to be modified by hypo and hyperthyroidism, but was increased by RA administration; (2) none of the administered treatments did alter CGRP mRNA level, whereas all of them influenced the axotomy-induced changes of motoneuron phenotype; (3) in hyperthyroid rats ChAT mRNA level of lumbar motoneurons not reduced homolateral to lesion while the number of ChAT-IR profiles was pronouncedly reduced; (4) up-regulation of p75 induced by peripheral nerve lesion was reduced in RA-treated rats. These data indicate that the motoneuron phenotype is regulated by transcription factors, which also play a role in phenotype switch regulation after axotomy.
ISSN:	0006-8993 1872-6240