Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Jun 3:9:194.
doi: 10.3389/fncel.2015.00194. eCollection 2015.

Possible role of glial cells in the relationship between thyroid dysfunction and mental disorders

Affiliations
Review

Possible role of glial cells in the relationship between thyroid dysfunction and mental disorders

Mami Noda. Front Cell Neurosci. .

Abstract

It is widely accepted that there is a close relationship between the endocrine system and the central nervous system (CNS). Among hormones closely related to the nervous system, thyroid hormones (THs) are critical for the development and function of the CNS; not only for neuronal cells but also for glial development and differentiation. Any impairment of TH supply to the developing CNS causes severe and irreversible changes in the overall architecture and function of the human brain, leading to various neurological dysfunctions. In the adult brain, impairment of THs, such as hypothyroidism and hyperthyroidism, can cause psychiatric disorders such as schizophrenia, bipolar disorder, anxiety and depression. Although impact of hypothyroidism on synaptic transmission and plasticity is known, its effect on glial cells and related cellular mechanisms remain enigmatic. This mini-review article summarizes how THs are transported into the brain, metabolized in astrocytes and affect microglia and oligodendrocytes, demonstrating an example of glioendocrine system. Neuroglial effects may help to understand physiological and/or pathophysiological functions of THs in the CNS and how hypo- and hyper-thyroidism may cause mental disorders.

Keywords: microglia; migration; phagocytosis; thyroid hormones; triiodothyronine.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Transport of THs to the brains and their metabolism. D: iodothyronine deiodinases, LAT: L-type amino acid transporter, MCT: monocarboxylate transporter, OATP: organic anion-transporting polypeptide, T2: diiodothyronines, T3: triiodothyronine, T4: thyroxine, TR: thyroid hormone receptor.
Figure 2
Figure 2
T3-induced signal transduction in microglia. NOS: Nitric oxide synthase, NCX: Na+/Ca2+ exchanger. (Modified from Mori et al., 2015).

References

    1. Awad A. G. (2000). The thyroid and the mind and emotions/thyroid dysfunction and mental disorders. Thyrobulletin 7, 3.e1–3.e2.
    1. Baxi E. G., Schott J. T., Fairchild A. N., Kirby L. A., Karani R., Uapinyoying P., et al. . (2014). A selective thyroid hormone beta receptor agonist enhances human and rodent oligodendrocyte differentiation. Glia 62, 1513–1529. 10.1002/glia.22697 - DOI - PMC - PubMed
    1. Becher B., Prat A., Antel J. P. (2000). Brain-immune connection: immuno-regulatory properties of CNS-resident cells. Glia 29, 293–304. 10.1002/(sici)1098-1136(20000215)29:4<293::aid-glia1>3.3.co;2-1 - DOI - PubMed
    1. Bernal J., Nunez J. (1995). Thyroid hormones and brain development. Eur. J. Endocrinol. 133, 390–398. 10.1530/eje.0.1330390 - DOI - PubMed
    1. Billon N., Tokumoto Y., Forrest D., Raff M. (2001). Role of thyroid hormone receptors in timing oligodendrocyte differentiation. Dev. Biol. 235, 110–120. 10.1006/dbio.2001.0293 - DOI - PubMed

LinkOut - more resources