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

Giardino, Luciana; Giuliani, Alessandro; Bettelli, Carla; Calzà, Laura

doi:10.1016/s0006-8993(01)03266-8

Cited by 7 publications

(4 citation statements)

References 63 publications

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“…This can result in a loss of functioning motor units, likely due to the overstimulation of motoneuron metabolism in patients with thyrotoxicosis [22]. Additionally, TH can reduce the number of choline acetyltransferase (ChAT)-immunoreactive neurons in the lumbar tract of the spinal cord by regulating gene transcription in hyperthyroid rats [23]. Furthermore, in hyperthyroid rats, the amplitude of miniature end-plate potentials and muscle-membrane potential were significantly reduced, and some muscle fibers were inexcitable even to direct stimulation [24].…”

Section: Discussionmentioning

confidence: 99%

Pathogenic SCN5A Mutation and Thyrotoxicosis-Related Neurological Syndrome: Casual or Causal Relationship?

Zhao

Jiang

et al. 2023

Brain Sciences

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Background: Various neurologic complications of hyperthyroidism are reported, and most of these complications are reversible with the amelioration of thyrotoxicosis. We report a previously undescribed concurrence of hyperthyroid-associated exercise-induced myalgia and stiffness, pyramidal tract dysfunction, and myoclonic movements that make an initial clinical diagnosis difficult. Case presentation: A 17-year-old male was hospitalized in the department of neurology, presenting with a 4-year history of severe exercise-induced myalgia and stiffness, weakness of lower limbs, and myoclonic movements. Laboratory investigations unexpectedly revealed hyperthyroidism. MRI of the brain and spine, electrophysiology, and whole exome sequencing were also performed. Antithyroid therapy led to marked improvement of neurologic symptoms, accompanied by a significant improvement of the time-dependent decline in compound muscle action potentials (CMAP) amplitudes after exercise and normalization of the prolonged QTc interval. Genetic analysis identified a rare variant in SCN5A. Conclusion: This case report provides important insights into the relationship between hyperthyroidism and neurologic/cardiac complications, particularly in those with a genetic predisposition. SCN5A mutation possibly plays a role in the complex neurological syndrome associated with hyperthyroidism. Further studies are warranted to better understand the underlying mechanisms and potential therapeutic options for these complex conditions.

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Section: Discussionmentioning

confidence: 99%

Pathogenic SCN5A Mutation and Thyrotoxicosis-Related Neurological Syndrome: Casual or Causal Relationship?

Zhao

Jiang

et al. 2023

Brain Sciences

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“…Vitamin play essential roles in brain function such as energy production, 32,33 DNA/RNA synthesis/repair, 34 the synthesis of neurochemicals 35 and signalling molecules 36 . Vitamins are not synthesized endogenously and therefore have to be obtained from the diet.…”

Section: Discussionmentioning

confidence: 99%

“…Vitamin play essential roles in brain function such as energy production, 32,33 DNA/RNA synthesis/repair, 34 the synthesis of neurochemicals 35 and signalling molecules. 36 Vitamins are not synthesized endogenously and therefore have to be obtained from the diet. Here, we found some vitamin-like metabolites, including 7,8-dihydrobiopterin, 4-hydroxybenzoic acid, pyridoxamine and vitamin B2, were significantly upregulated in serum of METH addicts.…”

Section: Sex-specific Alteration Of Serum Metabolitesmentioning

confidence: 99%

Sex‐specific metabolic signatures in methamphetamine addicts

et al. 2022

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Methamphetamine (METH) is a commonly abused addictive psychostimulant, and METH-induced neurotoxic and behavioural deficits are in a sex-specific manner.However, there is lack of biomarkers to evaluate METH addiction in clinical practice, especially for gender differences. We utilized ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) to detect the serum metabolomics in METH addicts and controls, specially exploring the sex-specific metabolic alterations by METH abuse. We found that many differently expressed metabolites in METH addicts related to metabolisms of amino acid, energy, vitamin and neurological disorders. Further, METH abuse caused different patterns of metabolomics in a sex-specific manner. As to amino acid metabolism, L-phenylalanine, Ltryptophan and L-histidine in serum of male addicts and betaine in serum of female addicts were significantly changed by METH use. In addition, it seemed that purine and pyrimidine-related metabolites (e.g., xanthosine and adenosine 5 0 -monophosphate) in male and the metabolites of hormone (e.g., cortisol) and folate biosynthesis (e.g., 7,8-dihydrobiopterin and 4-hydroxybenzoic acid) in female were more sensitive to METH addiction. Our findings revealed that L-glutamic acid, L-aspartic acid, alphaketoglutarate acid and citric acid may be potential biomarkers for monitoring METH addiction in clinic. Considering sex-specific toxicity by METH, the metabolites of purine and pyrimidine metabolism in male and those of stress-related hormones in female may be used to facilitate the accurate diagnosis and treatment for METH addicts of different genders.

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“…Finally, we should consider the possibility that part of the alterations observed in hypo‐ and hyperthyroid animals in NSCs and OPCs maturation, such as in the expression of oligodendrocyte markers, could be a result of an in vivo indirect effect through astrocytes or neurons. Our laboratory has provided extensive evidences on the role of thyroid hormone in maintaining neural and glial phenotype in adult brain (Calzà et al ., 1997a; 1998b), also acting on the regulation of growth factor synthesis (Calzà et al ., 1996; 1997b; Giardino et al ., 2002). However, post‐mitotic oligodendrocytes contain about the same number of TR binding sites per cell as neurons, i.e.…”

Section: Discussionmentioning

confidence: 99%

Thyroid hormone participates in the regulation of neural stem cells and oligodendrocyte precursor cells in the central nervous system of adult rat

Fernández

Pirondi

Manservigi

et al. 2004

Eur J of Neuroscience

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Oligodendrocyte development and myelination are under thyroid hormone control. In this study we analysed the effects of chronic manipulation of thyroid status on the expression of a wide spectrum of oligodendrocyte precursor cells (OPCs) markers and myelin basic protein (MBP) in the subventricular zone (SVZ), olfactory bulb and optic nerve, and on neural stem cell (NSC) lineage in adult rats. Hypo- and hyperthyroidism were induced in male rats, by propyl-thio-uracil (PTU) and L-thyroxin (T4) treatment, respectively. Hypothyroidism increased and hyperthyroidism downregulated proliferation in the SVZ and olfactory bulb (Ki67 immunohistochemistry and Western blotting, bromodeoxyuridine uptake). Platelet-derived growth factor receptor alpha (PDGFalpha-R) and MBP mRNA levels decreased in the optic nerve of hypothyroid rats; the same also occurred at the level of MBP protein. Hyperthyroidism slightly upregulates selected markers such as NG2 in the olfactory bulb. The lineage of cells derived from primary cultures of NSC prepared from the forebrain of adult hypo- and hyperthyroid also differs from those derived from control animals. Although no difference of in vitro proliferation of NSCs was observed in the presence of epidermal growth factor, maturation of oligodendrocytes (defined by process number and length) was enhanced in hyperthyroidism, suggesting a more mature state than in control animals. This difference was even greater when compared with the hypothyroid group, the morphology of which suggested a delay in differentiation. These results indicate that thyroid hormone affects NSC and OPC proliferation and maturation also in adulthood.

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

Cited by 7 publications

References 63 publications

Pathogenic SCN5A Mutation and Thyrotoxicosis-Related Neurological Syndrome: Casual or Causal Relationship?

Pathogenic SCN5A Mutation and Thyrotoxicosis-Related Neurological Syndrome: Casual or Causal Relationship?

Sex‐specific metabolic signatures in methamphetamine addicts

Thyroid hormone participates in the regulation of neural stem cells and oligodendrocyte precursor cells in the central nervous system of adult rat

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