Evidence for Effects on Neurology and Behavior - BioInitiative Report

oth exposure systems; however, the hippocampus cholinergic pathway responded to pulsed, but
not to continuous-wave RFR. Dosimetry data from the frontal cortex showed a wide range of
local SARs in the frontal cortex (0.11-1.85 W/kg per mW/cm 2) depending on the exposure
system. Yet, exposure in both systems produced similar neurochemical responses in the frontal
cortex (30-40% decrease in HACU). More interestingly, in the striatum the local SAR was
approximately five times higher when the animals were exposed in the circular waveguide than
in the miniature anechoic chamber; however, the striatal cholinergic system responded when the
animal was exposed in the miniature anechoic chamber, but not in the circular waveguide. Since
the cholinergic innervations in the striatum are mostly from interneurons inside the brain
structure, these data would argue against a direct action of RFR on striatal cholinergic neurons
causing a decrease in HACU, e.g., a local heating by the radiation. Unless different brain areas
have different sensitivities to the direct effect of RFR, we could conclude that the effects of RFR
on HACU in the brain areas studied in our experiments originated from other sites in the brain or
body.
Neurotransmitter Receptors
Further experiments were conducted to investigate the effects of repeated RFR exposure on
the cholinergic systems in the brain. Muscarinic cholinergic receptors were studied using the
receptor-binding technique with 3 H-quinuclidinyl benzilate (QNB) as the ligand. These receptors
are known to change their properties after repeated perturbation of the cholinergic system and
that such changes can affect an animal's normal physiological functions [Overstreet and
Yamamura, 1979]. After ten daily sessions of RFR exposure (2450 MHz at an average whole
body SAR of 0.6 W/kg), the concentration of muscarinic cholinergic receptors changed in the
brain [Lai et al., 1989b]. Moreover, the direction of change depended on the acute effect of the
RFR. When animals were given daily sessions of 20-min exposure, which increased cholinergic
activity in the brain, a decrease in the concentration of the receptors was observed in the frontal
cortex and hippocampus. On the other hand, when animals were subjected to daily 45-min
exposure sessions that decreased cholinergic activity in the brain, an increase in the
concentration of muscarinic cholinergic receptors in the hippocampus resulted after repeated
exposure and no significant effect was observed in the frontal cortex. These data pointed to an
important conclusion that the long term biological consequence of repeated RFR-exposure
depended on the parameters of exposure. Further experiments showed that changes in
cholinergic receptors in the brain after repeated RFR exposure also depended on endogenous
opioids, because the effects could be blocked by pretreatment be<strong>for</strong>e each session of daily
exposure with the narcotic antagonist naltrexone [Lai et al., 1991]. Interestingly, changes in
neurotransmitter receptor concentration also have been reported in animals after a single episode
of exposure to RFR [Gandhi and Ross, 1987]. In the experiment rats were irradiated with 700-
MHz RFR at 15 mW/cm 2 to produce a rise in body temperature of 2.5 o C (~10 min) and in some
animals the temperature was allowed to return to normal (~50 min). Alpha-adrenergic and
muscarinic cholinergic receptors were assayed in different regions of the brain using 3 H-
clonidine and 3 H-QNB as ligands, respectively. No significant change in binding was observed
<strong>for</strong> both receptors studied at the time when the body temperature reached a 2.5 o C increase.
Decreases in 3 H-clonidine binding in the cerebral cortex, hypothalamus, striatum, and
hypothalamus, and an increase in 3 H-QNB binding in the hypothalamus were observed when the
brains were studied at the time the body temperature returned to the base line level. The authors
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