(J Thorac Cardiovasc Surg 2012;144:S74-9)”
“Thyroid hormones (TH) are essential for normal brain MI-503 in vivo development. Even modest degrees of TH disruption experienced in utero can result in neuropsychological deficits in children despite normal thyroid status at birth. Neurotrophins have been implicated in a host of brain cellular functions, and in particular, brain-derived neurotrophic factor (BDNF) has a well documented role in development and function of the nervous system. A number of laboratories have reported the effects of TH administration or severe deprivation on neurotrophin expression in brain. This review provides an overview and update of recent developments in the thyroid

field as they relate to the nervous system. Secondly, we describe an animal model of low level TH insufficiency that is more relevant for studying the neurological consequences associated with the modest TH perturbations of subclinical hypothyroidism, or that would www.selleckchem.com/products/GDC-0449.html be anticipated

from exposure to environmental contaminants with a mode-of-action that involves the thyroid. Finally, we review the available in vivo literature on TH-mediated alterations in neurotrophins, particularly BDNF, and discuss their possible contribution to brain impairments associated with TH insufficiency. The observations of altered BDNF protein and gene expression have varied as a function of hypothyroid model, age, and brain region assessed. Only a handful of studies have investigated the relationship of neurotrophins and TH using models of TH deprivation that are not severe, and dose response information is sparse. Differences in the models used, species, doses, regions assessed, age at assessment, and method employed make it difficult to reach a consensus. Based on the available selleck products literature, the case for a direct role for BDNF in thyroid-mediated effects in the brain is not compelling. We conclude that delineation of the potential role of neurotrophins in TH-mediated neuronal development may be

more fruitful by examining additional neurotrophins (e.g., nerve growth factor), moderate degrees of TH insufficiency, and younger ages. We further suggest that investigation of BDNF invoked by synaptic activation (i.e., plasticity, enrichment, trauma) may serve to elucidate a role of thyroid hormone in BDNF-regulated synaptic function. This article is part of a Special Issue entitled: Steroid hormone actions in the CNS: the role of BDNF. Published by Elsevier Ltd. on behalf of IBRO.”
“The Nucleobase-Ascorbate Transporters (NATs) family includes carriers with fundamental functions in uptake of key cellular metabolites, such as uric acid or vitamin C. The best studied example of a NAT transporter is the uric acid-xanthine permease (UapA) from the model ascomycete Aspergillus nidulans.