Evidence for Effects on Neurology and Behavior - BioInitiative Report

(~3000 MHz) at 25 mW/cm 2 caused a decrease in AChE activity in the guinea pig brain. The
effect was most pronounced at the diencephalon and mesencephalon (midbrain). After three
months (3 h/day) of exposure at a power density of 3.5 mW/cm 2 , an increase in brain AChE was
observed. Surprisingly, when rabbits were subjected to the same chronic exposure treatment, a
decrease in AChE activity was seen. On the other hand, two groups of investigators [Galvin et
al., 1981; Miller et al., 1984] showed independently that 2450-MHz RFR exposure at a wide
range of SARs did not significantly affect the activity of isolated AChE in vitro. More recently,
Dutta et al. [1992] reported an increase in AChE activity in neuroblastoma cells in culture after
30 min of exposure to 147-MHz RFR amplitude-modulated at 16 Hz at SARs of 0.05 and 0.02
W/kg, but not at 0.005, 0.01, or 0.1 W/kg. The authors suggested a 'power window' effect. It is
not known whether the effect was a response to the radiofrequency or the 16-Hz component of
the radiation. Acetylcholinesterase is a very effective enzyme. A large decrease in its activity
will be needed be<strong>for</strong>e any change in cholinergic functions can be observed.
D'Inzeo et al. [1988] reported an experiment that showed the direct action of RFR on
acetylcholine-related ion channels in cultured chick embryo myotube cells. The acetylcholineinduced
opening and closing of a single channel in the membrane of these cells were studied by
the patch-clamp technique. Changes in membrane current of the whole cell in response to
acetylcholine was also studied. The channels were probably the nicotinic cholinergic receptor
channels, which are ligand-gated channels. The cell culture was exposed to continuous-wave
10750-MHz RFR with the power density at the cell surface estimated to be a few W/cm 2 .
(Power density of the incident field at the surface of the culture medium was 50 W/cm 2 .)
Recordings were made during exposure. The authors reported a decrease in acetylcholineactivated
single channel opening, whereas the duration of channel opening and the conductance
of the channels were not significantly affected by the radiation. Since these latter two parameters
are temperature-dependent, the effect observed was suggested as not related to the thermal
effects of RFR. The whole cell membrane current also showed an increase in the recovery rates
(desensitization) during irradiation. Thus, RFR decreased the opening probability of the
acetylcholine channel and increased the rate of desensitization of the acetylcholine receptors.
Opening and desensitization of the nicotinic channels are known to involve different molecular
mechanisms.
Lai et al. [1987b,c] per<strong>for</strong>med experiments to investigate the effects of RFR exposure on
the cholinergic systems in the brain of the rat. Activity of the two main cholinergic pathways,
septo-hippocampal and basalis-cortical pathways, were studied. The <strong>for</strong>mer pathway has the cell
bodies in the septum and their axons innervate the hippocampus. The latter pathway includes
neurons in the nucleus basalis and innervates several cortical areas including the frontal cortex.
These two cholinergic pathways are involved in many behavioral functions such as learning,
memory, and arousal [Steriade and Biesold, 1990]. Degeneration of these pathways occurs in
Alzheimers disease [Price et al., 1985]. In some studies, cholinergic activities in the striatum and
hypothalamus were also investigated. Cholinergic activity in the brain tissue was monitored by
measuring sodium-dependent high-affinity choline uptake (HACU) from brain tissues. Sodiumdependent
high-affinity choline is the rate limiting step in the synthesis of acetylcholine and has
widely been used as an index of cholinergic activity in neural tissue [Atweh et al., 1975].
We found that after 45 min of acute exposure to pulsed 2450-MHz RFR (2 s pulses, 500
pps, 1 mW/cm 2 , average whole body SAR 0.6 W/kg), HACU was decreased in the hippocampus
and frontal cortex, whereas no significant effect was observed in the striatum, hypothalamus, and
inferior colliculus [Lai et al., 1987b]. Interestingly, the effect of RFR on HACU in the
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