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Abstract
Microwaves have been proposed to alter neural functioning through both thermal and non-thermal mechanisms. We attempted to determine if local cerebral glucose utilization (LCGU) depends on the type of hyperthermic agent employed. We exposed the heads of rats to two different hyperthermic agents (5.6 GHz microwave exposure or exposure to hot/moist air) to create a 2°C rise in midbrain temperature. Other rats were sham exposed and remained normothermic. The 2-Deoxy-D-glucose (2DG) autoradiographic method was then used to determine LCGU during a 45-min period of stable hyperthermia. Hyperthermia (created by either hyperthermic agent) caused a general rise in brain glucose utilization. Hot-air exposed rats showed significantly higher LCGUs than microwaved rats in portions of the motor cortex, hypothalamus, lateral lemniscus and the substantia nigra (reticulata). Microwave exposure did not produce significantly higher levels of LCGU (compared to hot-air exposed hyperthermic controls) in any of the 47 brain areas sampled. A time analysis of lateral hypothalamic (LH) temperature during these different heating procedures revealed that microwave exposure produced a more-rapid rise in temperature than did hot/moist air. Thus, we wondered if the nuclei-specific differences in LCGU could be explained by localized differences in rate of brain heating during the two hyperthermic treatments. In a second study we carefully matched both the rate of lateral hypothalamic temperature rise and the peak temperatures achieved by our two hyperthermic methods and again measured LH LCGUs. We found that this precise matching eliminated the difference in hypothalamic LCGU previously observed following microwave or hot-air exposure. These data suggest that hyperthermia causes a general rise in brain metabolism and that (as long as steady state and rate of local brain temperature increase are well matched) microwave and hot-air induced hyperthermia produce similar changes in LCGU.