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Poirier, R.

Publications and source records attributed to Poirier, R..

2 recordsLinked to original sources

Repeated head-exposures to a 5G-3.5 GHz signal do not alter behavior but modify intracerebral gene expression in adult male mice.

The 5th generation (5G) of mobile communications promotes human exposures to electromagnetic fields exploiting the 3.5 GHz frequency band. We have analyzed behaviors, cognitive functions and gene expression in mice submitted to asymmetrical head-exposures to a 5G-modulated 3.5 GHz signal. The exposures were applied 1h daily, 5 days per week over a six-week period, at a specific absorption rate (SAR) averaging 0.19 W/kg over the brain. Locomotor activity in an open-field, object-place and object recognition memories were assessed repeatedly after four weeks of exposure and did not reveal any significant effect on the locomotion/exploration, anxiety level or memory processes. mRNA profiling was performed at the end of the exposure period in two symmetrical areas of the right and left cerebral cortex in which the SAR values were 0.43 and 0.14 W/kg, respectively. We found significant changes in the expression of less than 1% of the expressed genes with over-representations of genes related to glutamatergic synapses. The right cortical area differed from the left one by an over-representation of responsive genes encoded by the mitochondrial genome. Our data show that repeated head-exposures to a 5G-3.5 GHz signal can trigger mild transcriptome alterations without change in memory capacities or emotional state.

neuroscience↗

Hippocampal hypothyroidism in mice promotes glial cell activation and spatial memory deficits.

Adult-onset hypothyroidism is associated with learning and cognitive dysfunctions, which may be related to alterations in synaptic plasticity. Local reduced levels of thyroid hormones (THs) may impair glia morphology and activity, and promote the increase of pro-inflammatory cytokine levels mainly in the hippocampus. Given that neuroinflammation induces memory impairments, hypothyroidism-related glia dysfunction may participate in brain disorders. Thus, we investigated the mechanisms linking hypothyroidism, neuroinflammation and spatial memory, from a protective prospective. We induced hypothyroidism in adult C57BL/6J and wild-derived WSB/EiJ male mice by a seven-week propylthiouracil (PTU) treatment. We previously showed that WSB/EiJ mice were resistant to high-fat diet (HFD)-induced obesity, showing no neuroinflammatory response through adaptive abilities, unlike C57BL/6J. As PTU and HFD treatments are known to induce comparable inflammatory responses, we hypothesized WSB/EiJ mice might also be protected against hypothyroidism-induced neuroinflammation. We showed that hypothyroid WSB/EiJ mice depicted no hippocampal neuroinflammatory response and were able to maintain their hippocampal thyroid signalling despite low circulating TH levels. In contrast, C57BL/6J mice exhibited disturbed hippocampal TH signalling, accompanied by neuroinflammation and memory impairment. Our results reinforce the preponderance of local TH levels over circulating levels and the major role of hippocampal glia reactivity in the establishment of memory deficits.

neuroscience↗