Fetal radiofrequency radiation exposure from 800-1900 mhz-rated cellular telephones affects neurodevelopment and behavior in mice

Abstract

Neurobehavioral disorders are increasingly prevalent in children, however their etiology is not well understood. An association between prenatal cellular telephone use and hyperactivity in children has been postulated, yet the direct effects of radiofrequency radiation exposure on neurodevelopment remain unknown. Here we used a mouse model to demonstrate that in-utero radiofrequency exposure from cellular telephones does affect adult behavior. Mice exposed in-utero were hyperactive and had impaired memory as determined using the object recognition, light/dark box and step-down assays. Whole cell patch clamp recordings of miniature excitatory postsynaptic currents (mEPSCs) revealed that these behavioral changes were due to altered neuronal developmental programming. Exposed mice had dose-responsive impaired glutamatergic synaptic transmission onto layer V pyramidal neurons of the prefrontal cortex. We present the first experimental evidence of neuropathology due to in-utero cellular telephone radiation. Further experiments are needed in humans or non-human primates to determine the risk of exposure during pregnancy.

Figure 1. Behavioral testing in exposed and control mice.

The left column displays the data determined in mice at several ages after exposure. The right column demonstrates the cumulative average. To test memory the Standard object recognition memory test was used and a Preference Index (percent of total exploration time spent exploring the new object) shown at 8, 12, and 16 weeks of age. The cumulative mean preference index of the experimental group was 63.0% and the control group 69.9% (*p = 0.003, n = 161). To test hyperactivity we used the Light/Dark box test and display transitions at 12, 15, and 18 weeks of age. The cumulative mean number of transitions in the experimental group was 24.4 and the control group 16.4 (*p = <0.001, n = 141). To test anxiety we measured time spent in the dark at 12, 15, and 18 weeks of age. The cumulative average time spent in the dark in the experimental group was 207 seconds and in the control was 234 seconds (*p < 0.001, n = 141). To measure fear we used the Step down assay and display the time spent on the platform at 12 weeks and adulthood. The cumulative mean time spent on the platform in the experimental group was 16.7 seconds and in the control was 18.5 seconds (p = 0.59, n = 98).

Figure 2. Synaptic efficacy of glutamatergic synapses is decreased in brain neurons of mice after prenatal exposure to cell phone radiation.

A–C, mEPSCs were recorded in layer V pyramidal neurons of the prefrontal cortex. Representative traces of mEPSCs from control and cell phone exposure groups are shown in A. mEPSC frequency and cumulative probability of mEPSC amplitude from both groups are shown in B (*, P<0.05, t test) and C (**, P<0.01, Kolmogorov-Smirnov test; controls, 2225 events; Exposed, 2766 events). D–F, representative traces, frequency and amplitude of mEPSCs recorded in neurons in the VMH are shown. *, P<0.05, Kolmogorov-Smirnov test; Control: 2161 events, Cell phone group: 2261 events.

Figure 3. A dose-dependent attenuation in the frequency of mEPSCs in layer V pyramidal neurons in mice.

The frequency of mEPSCs recorded in mice prenatally exposed to cell phone radiation at of dose of 0, 9, 15 and 24 hrs per day are shown. Error bars are SEM. The dose responsive relationship is determined using regression analysis (Correlation coefficient, −0.97; r², 0.94; P<0.05).

Figure 4. Corticosterone levels during pregnancy were unaltered by exposure.

The mean corticosterone level in the pregnant control females was 69.94 ng/ml and in the exposed female mice was 69.91 ng/ml.