The hippocampus plays an important role in memory formation and cholinergic afferents appear to be integral to this phenomenon (Fibiger, 1991). It has long been understood that EEG recordings of theta activity made from the hippocampus are modulated by cholinergic activity (Smythe et al., 1992). There is considerable debate about the safety of mobile phone exposure for neuronal functioning; we reasoned that electromagnetic radiation (EMR) might be able to influence cognitive function when directed towards the temporal cortex containing the hippocampus. We reported that acute EMR exposure led to enhanced memory function in a short-term recall task (Smythe and Costall, 2003). These findings lead us to question whether or not EMR might directly influence hippocampal cholinergic activity and corresponding electrical activity as measured by theta. In the present study we have recorded hippocampal theta activity and large, irregular activity (LIA) prior to and following acute EMR exposure produced via a mobile phone and assayed cholinesterase activity to determine if cholinergic systems are influenced by mobile phones.

Ten, adult male and female rats (Lister Hooded) weighing 250-350g served as subjects. Hippocampal theta activity was performed under urethane anaesthesia (0.8g/ml ip; 1ml/kg). A hippocampal recording electrode was positioned in the stratum moleculare to record theta and LIA activities. Segments of EEG were recorded prior to and after a 15 min exposure to an active (receiving a call) mobile phone (Ericsson A2618s, 1800 MHz). The phone was positioned 3 cm above the head held in place in a stereotaxic frame. EEG signals were analysed by a computer-based FFT programme. A further 10 adult rats were exposed to either an inactive or active phone positioned above their cages for a period of 15 min and were then killed. The hippocampus was dissected out and subjected to a cholinesterase assay using commercially prepared kits (Sigma, Poole, UK). EEG data and cholinesterase activity were analysed by ANOVA.

Analysis revealed no effect of EMR on theta frequencies; however, there was a significant decline in the amplitude of the theta signal F(1, 6)= 8.2, P<.05. Pre-exposure amplitudes dropped from a mean (±SEM) of 367 (±85) µV to 275 (±58) µV. Moreover, LIA amplitudes measured at the peak theta frequency showed a significant increase F(1,6)= 8.4, P<.05. Pre-exposure values increased from 33 (±10) µV to post-exposure values of 67 (±18) µV. Animals exposed to an active mobile phone exhibited a significant decline in cholinesterase activity compared to those exposed to an inactive phone F(1, 8)= 7.3, P<.05. The formation of acetic acid metabolites in the assay fell from 2 µM/min to approximately 0.8 µM/min.

These data suggest that EMR emitted from a mobile phone are sufficiently powerful to alter ongoing electrical brain activity and corresponding neurochemical function. Whether or not these effects are harmful in the long term remains to be elucidated.

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Smythe, J.W. and Costall, B. (2003) NeuroReport, 14, 243-246.
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