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
. 2014 Jun 24:5:98.
doi: 10.3389/fendo.2014.00098. eCollection 2014.

Transport of thyroid hormone in brain

Affiliations
Review

Transport of thyroid hormone in brain

Eva K Wirth et al. Front Endocrinol (Lausanne). .

Abstract

Thyroid hormone (TH) transport into the brain is not only pivotal for development and differentiation, but also for maintenance and regulation of adult central nervous system (CNS) function. In this review, we highlight some key factors and structures regulating TH uptake and distribution. Serum TH binding proteins play a major role for the availability of TH since only free hormone concentrations may dictate cellular uptake. One of these proteins, transthyretin is also present in the cerebrospinal fluid (CSF) after being secreted by the choroid plexus. Entry routes into the brain like the blood-brain-barrier (BBB) and the blood-CSF-barrier will be explicated regarding fetal and adult status. Recently identified TH transmembrane transporters (THTT) like monocarboxylate transporter 8 (Mct8) play a major role in uptake of TH across the BBB but as well in transport between cells like astrocytes and neurons within the brain. Species differences in transporter expression will be presented and interference of TH transport by endogenous and exogenous compounds including endocrine disruptors and drugs will be discussed.

Keywords: Mct8; blood–brain-barrier; deiodinase; endocrine disruptors; flavonoids; l-type amino acid transporter; organic anion transporters; transthyretin.

PubMed Disclaimer

References

    1. Farwell AP, Dubord-Tomasetti SA, Pietrzykowski AZ, Stachelek SJ, Leonard JL. Regulation of cerebellar neuronal migration and neurite outgrowth by thyroxine and 3,3′,5′-triiodothyronine. Brain Res Dev Brain Res (2005) 154(1):121–3510.1016/j.devbrainres.2004.07.016 - DOI - PubMed
    1. Visser TJ, Leonard JL, Kaplan MM, Larsen PR. Kinetic evidence suggesting two mechanisms for iodothyronine 5′-deiodination in rat cerebral cortex. Proc Natl Acad Sci U S A (1982) 79(16):5080–410.1073/pnas.79.16.5080 - DOI - PMC - PubMed
    1. Verhoelst CH, Roelens SA, Darras VM. Role of spatiotemporal expression of iodothyronine deiodinase proteins in cerebellar cell organization. Brain Res Bull (2005) 67(3):196–20210.1016/j.brainresbull.2005.06.030 - DOI - PubMed
    1. Lemkine GF, Raj A, Alfama G, Turque N, Hassani Z, Alegria-Prevot O, et al. Adult neural stem cell cycling in vivo requires thyroid hormone and its alpha receptor. FASEB J (2005) 19(7):863–510.1096/fj.04-2916fje - DOI - PubMed
    1. Bernal J, Pekonen F. Ontogenesis of the nuclear 3,5,3′-triiodothyronine receptor in the human fetal brain. Endocrinology (1984) 114(2):677–910.1210/endo-114-2-677 - DOI - PubMed