Untitled

Makii, E. A.; Nerush, P. A.; Rodinskii, A. G.; Myakoushko, V. A.

doi:10.1023/a:1020218008768

Cited by 10 publications

(4 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Numerous studies have shown that thyroid hormones, including T4, regulate many aspects of neurogenesis, including proliferation, survival, migration, differentiation and maturation of neuronal and glial cells [ 2 , 88 , 89 , 90 ]. Furthermore, various studies indicate a modulatory role of thyroid hormones in neuronal excitability [ 91 , 92 , 93 , 94 ]. Finally, in the adult nervous system, T4 has been shown to have a neuroprotective effect and promote regeneration in experimental models of trauma [ 95 ].…”

Section: Thyroid Hormones and Vestibular Compensation In Animal Model...mentioning

confidence: 99%

“…Restoration of a physiological level of excitability of the neural network in the deafferented vestibular environment is a crucial parameter for vestibular compensation [ 80 , 85 , 86 ]. Various studies indicate a modulatory role of thyroid hormones on neuronal excitability [ 91 , 92 , 93 , 94 ]. High doses of T3 or T4 have been shown to act through a direct action on GABA A receptors by reducing GABAergic postsynaptic inhibitory currents in cultured hippocampal neurons [ 103 , 104 ].…”

Section: Thyroid Hormones and Vestibular Compensation In Animal Model...mentioning

confidence: 99%

“…In the zebrafish model, the rapid increase in voltage-dependent sodium currents in neurons by T4 requires both αVβ3 and Nav1.6a membrane receptors [ 105 , 106 ]. Thyroid hormones have also been shown to increase the excitability of the peripheral nervous system (sciatic nerve) [ 92 ] and neuronal discharge rates in cats [ 107 ]. Finally, electrophysiological findings in an Alzheimer’s rat model demonstrated that thyroid hormones increased spontaneous neuronal activity in the dentate gyrus [ 94 ].…”

Section: Thyroid Hormones and Vestibular Compensation In Animal Model...mentioning

confidence: 99%

See 2 more Smart Citations

Thyroid Axis and Vestibular Physiopathology: From Animal Model to Pathology

Rastoldo

Tighilet

2023

IJMS

View full text Add to dashboard Cite

A recent work of our group has shown the significant effects of thyroxine treatment on the restoration of postural balance function in a rodent model of acute peripheral vestibulopathy. Based on these findings, we attempt to shed light in this review on the interaction between the hypothalamic–pituitary–thyroid axis and the vestibular system in normal and pathological situations. Pubmed database and relevant websites were searched from inception through to 4 February 2023. All studies relevant to each subsection of this review have been included. After describing the role of thyroid hormones in the development of the inner ear, we investigated the possible link between the thyroid axis and the vestibular system in normal and pathological conditions. The mechanisms and cellular sites of action of thyroid hormones on animal models of vestibulopathy are postulated and therapeutic options are proposed. In view of their pleiotropic action, thyroid hormones represent a target of choice to promote vestibular compensation at different levels. However, very few studies have investigated the relationship between thyroid hormones and the vestibular system. It seems then important to more extensively investigate the link between the endocrine system and the vestibule in order to better understand the vestibular physiopathology and to find new therapeutic leads.

show abstract

Section: Thyroid Hormones and Vestibular Compensation In Animal Model...mentioning

confidence: 99%

Section: Thyroid Hormones and Vestibular Compensation In Animal Model...mentioning

confidence: 99%

Section: Thyroid Hormones and Vestibular Compensation In Animal Model...mentioning

confidence: 99%

See 1 more Smart Citation

Thyroid Axis and Vestibular Physiopathology: From Animal Model to Pathology

Rastoldo

Tighilet

2023

IJMS

View full text Add to dashboard Cite

show abstract

“…Clinical electroencephalographic (EEG) data indicate that hypothyroid patients display a slowing of the α-rhythm, evoked potentials, and peripheral conduction velocity [23][24][25], as well as a characteristic slowing of the speed of speech [26]. As result of the central hypothyroid status, both peripheral and cortical excitability are reduced simultaneously [27][28][29][30][31]. Since hypothyroidism is characterized by slowed neuronal function, we previously investigated whether thyroid hormone regulates neuronal Na + current density, which is the main determinant of the action potential upstroke velocity and also determines neuronal conduction velocity.…”

Section: Introductionmentioning

confidence: 99%

Deficiency of Thyroid Hormone Reduces Voltage-Gated Na+ Currents as Well as Expression of Na+/K+-ATPase in the Mouse Hippocampus

Sundaram

Marx²,

Lesslich³

et al. 2022

IJMS

View full text Add to dashboard Cite

Mice lacking functional thyroid follicular cells, Pax8−/− mice, die early postnatally, making them suitable models for extreme hypothyroidism. We have previously obtained evidence in postnatal rat neurons, that a down-regulation of Na+-current density could explain the reduced excitability of the nervous system in hypothyroidism. If such a mechanism underlies the development of coma and death in severe hypothyroidism, Pax8−/− mice should show deficits in the expression of Na+ currents and potentially also in the expression of Na+/K+-ATPases, which are necessary to maintain low intracellular Na+ levels. We thus compared Na+ current densities in postnatal mice using the patch-clamp technique in the whole-cell configuration as well as the expression of three alpha and two beta-subunits of the Na+/K+-ATPase in wild type versus Pax8−/− mice. Whereas the Na+ current density in hippocampal neurons from wild type mice was upregulated within the first postnatal week, the Na+ current density remained at a very low level in hippocampal neurons from Pax8−/− mice. Pax8−/− mice also showed significantly decreased protein expression levels of the catalytic α1 and α3 subunits of the Na+/K+-ATPase as well as decreased levels of the β2 isoform, with no changes in the α2 and β1 subunits.

show abstract

Peripheral and central administration of T3 improved the histological changes, memory and the dentate gyrus electrophysiological activity in an animal model of Alzheimer’s disease

et al. 2017

View full text Add to dashboard Cite

The amyloid beta (Aβ) induced Alzheimer's disease (AD) is associated with formation the amyloid plaques, cognitive impairments and decline in spontaneous discharge of neurons. In the current study, we evaluated the effect of subcutaneous (S. C) and intrahippocampal (I. H) administrations of triiodothyronine (T3) on the histological changes, memory and the dentate gyrus (DG) electrophysiological activity in an animal model of AD. Eighty adult male Wistar rats (250-300 g) were divided randomly into five groups: Sham-Operated (Sh-O), AD + Vehicle (S. C), AD + Vehicle (I. H), AD+ T3 (S. C) and AD + T3 (I. H). In order to induce animal model of AD, Aβ (10 ng/μl, bilaterally) were injected intrahippocampally. Rats were treated with T3 and/or normal saline for 10 days. Passive avoidance and spatial memory were evaluated in shuttle box apparatus and Morris water maze, respectively. Neuronal single unit recording was assessed from hippocampal DG. The percent of total time that animals spent in target quarter, the mean latency time (sec), the step through latency and the average number of spikes/bin were decreased significantly in AD rats compared with the Sh-O group (p < 0.001) and were increased significantly in AD groups that have received T3 (S. C and I. H) in compared with AD group (p < 0.01, p < 0.001). Also, formation of amyloid plaques was decreased in AD rats treated with T3.The results showed that T3 injection (S. C and I. H), by reduction of neural damage and increment of neuronal spontaneous activity improved the memory deficits in Aβ-induced AD rats.

show abstract

Untitled

Cited by 10 publications

References 11 publications

Thyroid Axis and Vestibular Physiopathology: From Animal Model to Pathology

Thyroid Axis and Vestibular Physiopathology: From Animal Model to Pathology

Deficiency of Thyroid Hormone Reduces Voltage-Gated Na+ Currents as Well as Expression of Na+/K+-ATPase in the Mouse Hippocampus

Peripheral and central administration of T3 improved the histological changes, memory and the dentate gyrus electrophysiological activity in an animal model of Alzheimer’s disease

Contact Info

Product

Resources

About