Microwave attenuation of ethanol-induced interactions with noradrenergic neurotransmitter systems

Research suggests that microwave (MW) irradiation can attenuate ethanol (EtOH)-induced hypothermia in a manner that may depend, in part, on noradrenergic (NE) neurotransmitter systems. To investigate this possible interaction, neonatal rats were injected with the neurotoxin 6-hydroxydopamine (6-OHDA) to lesion central NE neurons. When tested as adults, lesioned, MW irradiated rats did not demonstrate the interaction between MW (2.45 GHz, 45 min, specific absorption rate = 0.3 W/kg) and EtOH-induced hypothermia that was seen among control animals. Additional experiments examined MW interactions with centrally and peripherally acting beta-adrenergic antagonists. Acute low-level MW irradiation attenuated EtOH-induced hypothermia in the rat. Pretreatment with 1.0 mg/kg of the centrally active beta-adrenergic antagonist propranolol significantly attenuated the ethanol-induced hypothermia of sham-irradiated (SH-irradiated) rats. There was no consistent effect of propranolol on MW irradiated animals, regardless of dose. Similarly, the degree of hypothermia demonstrated by SH-irradiated controls was significantly attenuated compared to MW irradiated animals by pretreatment with the peripheral beta-adrenergic antagonist CGP-12177 (doses of 0.1, 1.0 and 10.0 mg/kg). In vivo binding data indicates only the highest dose of CGP-12177 to be centrally active. Taken together, the results confirm NE mediation of EtOH-induced hypothermia and suggest that MW energy may in some way mimic the role of beta-adrenergic antagonists.