Thyroid Hormone Effects on Sensory Perception, Mental Speed, Neuronal Excitability and Ion Channel Regulation

Dietzel, Irmgard D.; Mohanasundaram, Sivaraj; Niederkinkhaus, Vanessa; Hoffmann, Gerhard; Meyer, Jens; Reiners, Christoph; Blasl, Christiana; Bohr, Katharina

doi:10.5772/48310

Cited by 3 publications

(2 citation statements)

References 200 publications

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“…Since increases in Na þ channel density in the membrane lead to increases in conduction velocity for channel densities up to 2000 channels mm 22 [66], this furthermore leads to an acceleration of information processing in the brain allowing animals to react faster to various challenges. As discussed in [67], this might be a mechanism by which thyroid hormone speeds up many functions of the nervous system, including speech and visual perception.…”

Section: Discussionmentioning

confidence: 99%

Regulation of neuronal excitability by release of proteins from glial cells

Igelhorst

Niederkinkhaus

Karus

et al. 2015

Phil. Trans. R. Soc. B

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Effects of glial cells on electrical isolation and shaping of synaptic transmission between neurons have been extensively studied. Here we present evidence that the release of proteins from astrocytes as well as microglia may regulate voltage-activated Na þ currents in neurons, thereby increasing excitability and speed of transmission in neurons kept at distance from each other by specialized glial cells. As a first example, we show that basic fibroblast growth factor and neurotrophin-3, which are released from astrocytes by exposure to thyroid hormone, influence each other to enhance Na þ current density in cultured hippocampal neurons. As a second example, we show that the presence of microglia in hippocampal cultures can upregulate Na þ current density. The effect can be boosted by lipopolysaccharides, bacterial membrane-derived stimulators of microglial activation. Comparable effects are induced by the exposure of neuron-enriched hippocampal cultures to tumour necrosis factor-a, which is released from stimulated microglia. Taken together, our findings suggest that release of proteins from various types of glial cells can alter neuronal excitability over a time course of several days. This explains changes in neuronal excitability occurring in states of thyroid hormone imbalance and possibly also in seizures triggered by infectious diseases.

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Section: Discussionmentioning

confidence: 99%

Regulation of neuronal excitability by release of proteins from glial cells

Igelhorst

Niederkinkhaus

Karus

et al. 2015

Phil. Trans. R. Soc. B

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“…In spite of the fact that hypothyroidism can currently be prevented by controlled hormone substitution, the molecular mechanisms responsible for the characteristic mental slowdown remain elusive [17][18][19][20][21][22]. 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].…”

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

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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.

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Effect on Reaction Time in Primary Hypothyroid Patients Before and After Thyroxin Treatment

Kale¹,

Katole²,

Rode³

et al. 2022

Cureus

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Introduction Thyroid hormones play a crucial role in the proper functioning of the nervous system. Both T3 and T4 hormones have many significant actions on the neuromuscular system and brain. In hypothyroid patients, various neurological signs and symptoms such as weakness, fatigue, paresthesias, arthralgias, etc. may be seen. Reaction time is a good indicator of the processing of the central nervous system. So, our study aims to observe the change in reaction time in hypothyroid patients as compared to the control group. And to understand, if some difference is observed, how does it change after treatment with thyroxin in a hypothyroid group. Materials and methods This study was conducted at the tertiary care teaching hospital in the Vidarbha region. In this study, 40 newly diagnosed primary hypothyroid patients (including males and females), in the age group of 20 to 45 years, and whose thyroid-stimulating hormone (TSH) levels were between 10 and 50 mIU/L and free T4 levels below the normal level were included. A suitable comparable control group of the same demographic parameter was selected. Reaction time was taken before the start of thyroxin treatment in both groups, and results were analyzed by using an unpaired t-test. The reaction time of the hypothyroid group was again measured after eight weeks of the start of thyroxin treatment, it was compared with the initial reaction time, and data were compared by using the paired t-test. Result In the hypothyroid group as compared to the control group both auditory and visual reaction times were significantly on the higher side (p<0.05). Also, there was a significant improvement in reaction time after the start of thyroxin treatment (p<0.05), which suggests improvement in CNS activity in hypothyroid patients after initiation of therapy. Conclusion Thyroid hormones play a crucial role in the proper functioning and processing of the central nervous system. Due to this reason, reaction time in hypothyroid patients was on the longer side, showing a slowing of the nervous system when reacting to a specific stimulus. After thyroxin treatment for a sufficient period, reaction times were of shorter duration as compared to before the start of thyroxin, which shows well-recovered nervous activity. Therefore, reaction time is not only used as a handy tool to identify early central nervous system manifestations of hypothyroidism but also used to monitor response to treatment.

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Thyroid Hormone Effects on Sensory Perception, Mental Speed, Neuronal Excitability and Ion Channel Regulation

Cited by 3 publications

References 200 publications

Regulation of neuronal excitability by release of proteins from glial cells

Regulation of neuronal excitability by release of proteins from glial cells

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

Effect on Reaction Time in Primary Hypothyroid Patients Before and After Thyroxin Treatment

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