Effects of 900 MHz radiofrequency on corticosterone, emotional memory and neuroinflammation in middle-aged rats

International audienceThe widespread use of mobile phones raises the question of the effects of electromagnetic fields (EMF, 900 MHz) on the brain. Previous studies reported increased levels of the glial fibrillary acidic protein (GFAP) in the rat's brain after a single exposure to 900 MHz global system for mobile (GSM) signal, suggesting a potential inflammatory process. While this result was obtained in adult rats, no data is currently available in older animals. Since the transition from middle-age to senescence is highly dependent on environment and lifestyle, we studied the reactivity of middle-aged brains to EMF exposure. We assessed the effects of a single 15 min GSM exposure (900 MHz ; specific absorption rate (SAR)=6 W/kg) on GFAP expression in young adults (6 week-old) and middle-aged rats (12 month-old). Brain interleukin (IL)-1ß and IL-6, plasmatic levels of corticosterone (CORT), and emotional memory were also assessed. Our data indicated that, in contrast to previously published work, acute GSM exposure did not induce astrocyte activation. Our results showed an IL-1ß increase in the olfactory bulb and enhanced contextual emotional memory in GSM-exposed middle-aged rats, and increased plasmatic levels of CORT in GSMexposed young adults. Altogether, our data showed an age dependency of reactivity to GSM exposure in neuro-immunity, stress and behavioral parameters. Reproducing these effects and studying their mechanisms may allow a better understanding of mobile phone EMF effects on neurobiological parameters

Impact of cerebral radiofrequency exposures on oxidative stress and corticosterone in a rat model of Alzheimer's disease

Alzheimer´s diseases (AD) is the most common type of neurodegenerative disease leading to dementia. The cause of AD remains unknown, however several studies suggested that mobile phone radiofrequency electromagnetic fields (RF-EMF) exposures interacted with AD memory deficits in rodent models. Here we aimed to test the hypothesis that RF-EMF exposure may modify memory through corticosterone and oxidative stress in a rat model of AD. Long-Evans rats were healthy controls or AD models. AD rats received continuous intracerebroventricular infusion with ferrous sulphate, beta amyloid (βA) 1-42 peptide and buthionine-sufloximine (Lecanu, 2006). RF-EMF exposures were performed to the head for 1 month (5 days/week, 15 or 45 min/day in restraint) to mimic cell phone use. To look for hazard threshold, repeated exposures were set to reach high brain averaged specific absorption rates (BASAR): 1,5 W/Kg (15 min), 6 W/Kg (15 min) or 6 W/Kg (45 min). The sham group exposure was 0 W/kg (45 min). Endpoints were spatial memory in the radial maze, plasmatic corticosterone, heme oxygenase 1 (HO1) and neurofibrillary tangles. Results indicated that AD rats had increased thioflavine and HO1 staining, reduced memory performances and similar corticosterone level compared to healthy rats. In AD rats, reduced corticosterone and increased hippocampal HO1 staining were observed after the 6 W/kg 45 min exposure. There was no RF-EMF effect on memory and cortical HO1. In healthy rats, increased cortical HO1 staining was observed after the 6 W/kg 45 min exposure. There was no RF-EMF effect on memory, hippocampal HO1 staining or corticosterone. According to our data, neither AD nor healthy rats showed modified memory after RF-EMF exposures. Unlike healthy rats, AD rats showed higher hippocampal oxidative stress and reduced corticosterone after our highest BASAR exposures. This data may support the hypothesis of a specific fragility related to neurodegenerative disease towards RF-EMF exposures. Further studies should be performed to replicate this data

Neurobiological effects of repeated radiofrequency exposures in male senescent rats

International audienceThe increasing use of mobile phones by aging people raises issues about the effects of radiofrequency electromagnetic fields (RF-EMF) on the aging central nervous system. Here, we tested if mobile phone RF-EMF exposures could exacerbate senescence-typical neurobiological deficits. Thus, aged (22-24 months) and young (4-6 months) adult male rats were subjected to head RF-EMF exposures (900 MHz, specific absorption rate (SAR) of 6 W/kg, 45 min/day for 1 month in restraint rockets). To assess senescence-typical neurobiological deficits, spatial memory, emotional memory, anxiety-related behavior, locomotor activity, interleukins (IL)-1 beta and 6, glial fibrillary acidic protein (GFAP) and corticosterone were measured. Aged rats presented deficits in spatial learning, exploration, anxiety-related behaviors, and increased hippocampal ILs and cortical IL-1 beta Results showed that senescence-typical neurobiological deficits were not modified by RF-EMF exposures. RF-EMF-exposed rats (young and aged adults pooled) had decreased anxiety-related behaviors in the elevated plus maze. This study which is the first to assess RF-EMF exposures during late aging did not support the hypothesis of a specific cerebral vulnerability to RF-EMF during senescence. More investigations using longer RF-EMF exposures should be performed to conclude regarding the inoffensiveness of RF-EMF exposures

Effects of 900 MHz radiofrequency on corticosterone, emotional memory and markers of cerebral inflammation in middle-aged rats

This study aimed to assess if GSM exposure tested in middle aged rats was associated with changes in stress, cerebral function and biomarkers, in addition to GFAP increase previously demonstrated in adult rat brain. Results showed that GSM did not modify behavior and cytokines, while GFAP analysis is still in process. GSM-induced corticosterone increase was obtained with age differences, suggesting that GSM may be perceived as a stress in young animals but this process disappeared with ageing

Effets comportementaux et biochimiques des ondes radiofréquence du téléphone portable sur le rat âgé

PARIS7-Bibliothèque centrale (751132105) / SudocSudocFranceF

Impact of stress on electromagnetic field-induced corticosterone, cytokines and GFAP responses

The widespread use of mobile phones raises the question of the effects of electromagnetic fields (EMF, 900 MHz) on the brain. Experimentally, local brain EMF exposures are performed in rats maintained in contention in Plexiglas rockets. Previous studies reported increased levels of cerebral glial fibrillary acidic protein (GFAP) after a single EMF exposure, suggesting a potential inflammatory process. However, these effects were not always reproduced, and the present study aims to test the contribution of protocol-induced stress in EMF-induced responses. To do so, plasmatic levels of corticosterone, GFAP, interleukin (IL)-1ß and IL-6 were measured 48 h following a single, 15 min, (0 or 6 W/kg) EMF-exposure in rats subjected to fear conditioning and tests (group 1 and 2). Test of stress was performed by measuring the same biological responses 30 min, 5 h and 24 h following (group 3) daily handling, (groups 4 and 5) a single, 15 min, (0 or 6 W/kg) GSM-exposure, and (group 6) a single 15 min sham (0W/kg GSM)-exposure followed by a fear conditioning session. Results showed that corticosterone increase was found only in groups 2 and 6, and no effect on IL-1ß, IL-6 or GFAP was obtained. According to these data, stressful situation linked to fear conditioning procedure did not modify GFAP or IL responses. Moreover, according to corticosterone measure, acute 15 min contention did not appear as a stressful event in our study. The use of fear conditioning in our protocol and the demonstration that it increases corticosterone after 30 min must be highlighted as a possible interacting parameter. Identification of contention-linked side effects may allow a better understanding of mobile phone EMF effects on neurobiological parameters

Impact of Cerebral Radiofrequency Exposures on Oxidative Stress and Corticosterone in a Rat Model of Alzheimer's Disease

Background: Alzheimer's disease (AD) is the most common type of neurodegenerative disease leading to dementia. Several studies suggested that mobile phone radiofrequency electromagnetic field (RF-EMF) exposures modified AD memory deficits in rodent models. Objective: Here we aimed to test the hypothesis that RF-EMF exposure may modify memory through corticosterone and oxidative stress in the Samaritan rat model of AD. Methods: Long-Evans male rats received intracerebroventricular infusion with ferrous sulphate, amyloid-beta 1-42 peptide, and buthionine-sufloximine (AD rats) or with vehicle (control rats). To mimic cell phone use, RF-EMF were exposed to the head for 1 month (5 days/week, in restraint). To look for hazard thresholds, high brain averaged specific absorption rates (BASAR) were tested: 1.5 W/Kg (15 min), 6 W/Kg (15 min), and 6 W/Kg (45 min). The sham group was in restraint for 45 min. Endpoints were spatial memory in the radial maze, plasmatic corticosterone, heme oxygenase-1 (HOl), and amyloid plaques. Results: Results indicated similar corticosterone levels but impaired memory performances and increased cerebral staining of thioflavine and of HOl in the sham AD rats compared to the controls. A correlative increase of cortical HOl staining was the only effect of RF-EMF in control rats. In AD rats, RF-EMF exposures induced a correlative increase of hippocampal HO1 staining and reduced corticosterone. Discussion: According to our data, neither AD nor control rats showed modified memory after RF-EMF exposures. Unlike control rats, AD rats showed higher hippocampal oxidative stress and reduced corticosterone with the higher BASAR. This data suggests more fragility related to neurodegenerative disease toward RF-EMF exposures

Neurobiological effects of repeated radiofrequency exposures in male senescent rats

The increasing use of mobile phones by aging people raises issues about the effects of radiofrequency electromagnetic fields (RF-EMF) on the aging central nervous system. Here, we tested if mobile phone RF-EMF exposures could exacerbate senescence-typical neurobiological deficits. Thus, aged (22–24 months) and young (4–6 months) adult male rats were subjected to head RF-EMF exposures (900 MHz, specific absorption rate (SAR) of 6 W/kg, 45 min/day for 1 month in restraint rockets). To assess senescence-typical neurobiological deficits, spatial memory, emotional memory, anxiety-related behavior, locomotor activity, interleukins (IL)-1β and 6, glial fibrillary acidic protein and corticosterone were measured. Aged rats presented deficits in spatial learning, exploration, anxiety-related behaviors, and increased hippocampal ILs and cortical IL-1β. Results showed that senescence-typical neurobiological deficits were not modified by RF-EMF exposures. RF-EMF-exposed rats (young and aged adults pooled) had decreased anxiety-related behaviors in the elevated plus maze. This study which is the first to assess RF-EMF exposures during late aging did not support the hypothesis of a specific cerebral vulnerability to RF-EMF during senescence. More investigations using longer RF-EMF exposures should be performed to conclude regarding the inoffensiveness of RF-EMF exposures

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

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

Impact of dose and duration of GSM exposure on GFAP, myelin basic protein, beta amyloid 1-40 and emotional memory

This study aimed to assess if GSM exposure (1.5W/kg-15min, 6W/kg-15 and 45min) was associated with further changes in cerebral function and biomarkers, in addition to glial fibrillary acidic protein (GFAP) increase previously demonstrated in the rat brain. Results showed a partial reproducibility on GFAP levels. Further biological responses were not dependent on SAR or exposure duration. These results strongly support the complexity of electromagnetic fields effect on biological responses and point out the need to assess the parameters of its variability