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Thyroid hormone and astroglia: endocrine control of the neural environment.
J Neuroendocrinol
June 2015
Instituto de Ciências Biomédicas, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Thyroid hormones (THs) play key roles in brain development and function. The lack of THs during childhood is associated with the impairment of several neuronal connections, cognitive deficits and mental disorders. Several lines of evidence point to astrocytes as TH targets and as mediators of TH action in the central nervous system; however, the mechanisms underlying these events are still not completely known.
View Article and Find Full Text PDFChanges in dialysate concentrations of glutamate and GABA in the brain: an index of volume transmission mediated actions?
J Neurochem
April 2003
Department of Physiology, Faculty of Medicine, University Complutense, Madrid, Spain.
Brain microdialysis has become a frequently used method to study the extracellular concentrations of neurotransmitters in specific areas of the brain. For years, and this is still the case today, dialysate concentrations and hence extracellular concentrations of neurotransmitters have been interpreted as a direct index of the neuronal release of these specific neurotransmitter systems. Although this seems to be the case for neurotransmitters such as dopamine, serotonin and acetylcholine, the extracellular concentrations of glutamate and GABA do not provide a reliable index of their synaptic exocytotic release.
View Article and Find Full Text PDFMotor neurones in culture as a model to study ALS.
J Neurol
March 2000
The Institute of Neurology, University of Milan Medical School, I.R.C.C.S. Maggiore Hospital, Italy.
Defining the basis of the selective cell vulnerability of motor neurones (MN) represents the key issue in amyotrophic lateral sclerosis (ALS), and tissue culture models are the ideal system for the identification of the MN specific features at the single cell level. Neurone-astrocyte metabolic interactions, which have a critical role in MN through glutamatergic toxicity, have been mostly defined in vitro. Ca++ metabolism, which appears to play a critical role in inducing MN loss in ALS, has been successfully studied using in vitro cell models.
View Article and Find Full Text PDFGlucocorticoids up-regulate the expression of glial fibrillary acidic protein in the rat suprachiasmatic nucleus.
Glia
February 2000
Interactions Fonctionnelles en Neuroendocrinologie, INSERM, Institut Fédératif Jean-Roche, Université de la Méditerranée, Marseille, France.
Immunoreactivity against glial fibrillary acidic protein (GFAP) was used as a dynamic index in adrenalectomized rats subjected or not to corticosterone replacement to investigate whether glucocorticoids may interact with astrocytes in the suprachiasmatic nucleus (SCN), the master component of the central circadian clock. GFAP staining in the SCN was significantly higher in rats having received implants that restored physiological plasma levels of corticosterone within diurnal or nocturnal limits than in non-normalized rats. The effects of corticosterone were similar in the parvocellular portion of the paraventricular nucleus but were opposite in the hippocampus, another major site of negative feed-back regulation of the hypothalamic-pituitary-adrenal axis, where a decreased GFAP staining was observed in discrete regions of the dentate gyrus.
View Article and Find Full Text PDFMotor neurone metabolism.
J Neurol Sci
October 1999
The Institute of Neurology, University of Milan Medical School, IRCCS Maggiore Hospital, Via. F. Sforza 35, 20122, Milano, Italy.
The cell and molecular mechanisms which determine the motor neurone (MN) phenotype are unclear. Tissue culture models offer a unique system for the study of a wide variety of MN features. For instance, since the neurone-astrocyte metabolic interactions play a critical role in the selective MN loss observed in amyotrophic lateral sclerosis (ALS), the glutamatergic MN toxicity could be reanalyzed in vitro, after a careful evaluation of the role of astrocytes.
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