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Glial markers and emotional memory in rats following acute cerebral radiofrequency exposures.

作者信息

Barthélémy Amélie, Mouchard Amandine, Bouji Marc, Blazy Kelly, Puigsegur Renaud, Villégier Anne-Sophie

机构信息

Institut national de l'environnement industriel et des risques (INERIS), Unité de Toxicologie Expérimentale, Parc Technologique ALATA, BP no. 2, 60550, Verneuil-en-Halatte, France.

Institut des Neurosciences Cellulaires et Intégratives, CNRS UPR 3212, 5 rue Blaise Pascal, 67084, Strasbourg, France.

出版信息

Environ Sci Pollut Res Int. 2016 Dec;23(24):25343-25355. doi: 10.1007/s11356-016-7758-y. Epub 2016 Sep 30.


DOI:10.1007/s11356-016-7758-y
PMID:27696165
Abstract

The widespread mobile phone use raises concerns on the possible cerebral effects of radiofrequency electromagnetic fields (RF EMF). Reactive astrogliosis was reported in neuroanatomical structures of adaptive behaviors after a single RF EMF exposure at high specific absorption rate (SAR, 6 W/kg). Here, we aimed to assess if neuronal injury and functional impairments were related to high SAR-induced astrogliosis. In addition, the level of beta amyloid 1-40 (Aβ 1-40) peptide was explored as a possible toxicity marker. Sprague Dawley male rats were exposed for 15 min at 0, 1.5, or 6 W/kg or for 45 min at 6 W/kg. Memory, emotionality, and locomotion were tested in the fear conditioning, the elevated plus maze, and the open field. Glial fibrillary acidic protein (GFAP, total and cytosolic fractions), myelin basic protein (MBP), and Aβ1-40 were quantified in six brain areas using enzyme-linked immunosorbent assay. According to our data, total GFAP was increased in the striatum (+114 %) at 1.5 W/kg. Long-term memory was reduced, and cytosolic GFAP was increased in the hippocampus (+119 %) and in the olfactory bulb (+46 %) at 6 W/kg (15 min). No MBP or Aβ1-40 expression modification was shown. Our data corroborates previous studies indicating RF EMF-induced astrogliosis. This study suggests that RF EMF-induced astrogliosis had functional consequences on memory but did not demonstrate that it was secondary to neuronal damage.

摘要

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本文引用的文献

[1]
Cerebral radiofrequency exposures during adolescence: Impact on astrocytes and brain functions in healthy and pathologic rat models.

Bioelectromagnetics. 2016-7

[2]
Neurobiological effects of repeated radiofrequency exposures in male senescent rats.

Biogerontology. 2016-11

[3]
Lead Poisoning Disturbs Oligodendrocytes Differentiation Involved in Decreased Expression of NCX3 Inducing Intracellular Calcium Overload.

Int J Mol Sci. 2015-8-13

[4]
Oxidative stress caused by ozone exposure induces β-amyloid 1-42 overproduction and mitochondrial accumulation by activating the amyloidogenic pathway.

Neuroscience. 2015-9-24

[5]
Effect of long-term (2 years) exposure of mouse brains to global system for mobile communication (GSM) radiofrequency fields on astrocytic immunoreactivity.

Bioelectromagnetics. 2015-4

[6]
Effects of selenium on lead-induced alterations in Aβ production and Bcl-2 family proteins.

Environ Toxicol Pharmacol. 2014-12-10

[7]
17β-trenbolone, an anabolic-androgenic steroid as well as an environmental hormone, contributes to neurodegeneration.

Toxicol Appl Pharmacol. 2015-1-1

[8]
Exposure to As-, Cd-, and Pb-mixture induces Aβ, amyloidogenic APP processing and cognitive impairments via oxidative stress-dependent neuroinflammation in young rats.

Toxicol Sci. 2015-1

[9]
Differential pro-inflammatory responses of astrocytes and microglia involve STAT3 activation in response to 1800 MHz radiofrequency fields.

PLoS One. 2014-10-2

[10]
Plant toxin abrin induced oxidative stress mediated neurodegenerative changes in mice.

Neurotoxicology. 2014-9

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