VGCC activation has been shown to have a universal or near- universal role in the release of neurotransmitters in the brain and also in the release of hormones by neuroendocrine cells (Berridge, 1998; Dunlap et al., 1995; Wheeler et al., 1994), with such release being produced by calcium signaling. There are high densities of diverse VGCCs occurring in neurons throughout the nervous system. Both the high VGCC density and their function in neurotransmitter and neuroendocrine release throughout the nervous system suggests that the nervous system is likely to be highly sensitive to low intensity EMFs.
A wide variety of brain and peripheral nervous system tissues show histological changes following non-thermal exposures. Among the important tissues impacted are the hypothalamus and pituitary gland, where both show similar patterns of changes in neuroendocrine activities. There Is an initial increase in neuroendocrine activity (this may be produced directly by VGCC stimulation of secretion), followed over time by ‘‘exhaustion’’ of neuroendocrine activity (this may be produced by tissue damage produced from long term intracellular calcium [Ca2+]i elevation).
There are widespread histological changes produced in neuro- nal and neuroendocrine tissues. These were repeatedly reported to be largely reversible on cessation of EMF exposure. They become, however, irreversible when exposure is extended in time.
Elevated VGCC activity, produced by an allele of the CACNA1C gene which encodes the channel of the main L-type VGCC in the brain, produces various neuropsychiatric effects (Table 1). This predicts, that low intensity non-thermal microwave frequency EMFs which also produce elevated L-type and other VGCC activity, therefore produce widespread neuropsychiatric effects.