Microwave attenuation of ethanol-induced interactions with noradrenergic neurotransmitter systems med./bio.

Research suggests that microwave exposure can attenuate ethanol-induced hypothermia in a manner that may depend, in part, on noradrenergic neurotransmitter systems. To study this possible interaction, neonatal rats were injected with the neurotoxin 6-hydroxydopamine (6-OHDA) to lesion central noradrenergic neurons and to induce ethanol hypothermia as adults (experiment 1). Additional experiments investigated microwave interactions with centrally and peripherally acting beta-adrenergic antagonists (propranolol and CGP-12177) to antagonize ethanol-induced hypothermia in microwave exposed animals (experiments 2 and 3).

• animal
• rat/Long-Evans
• whole body

Experiment 1: When tested as adults, lesioned, microwave exposed rats did not show the interaction between microwave and ethanol-induced hypothermia that was seen among control rats. The data of experiment 1 suggest that microwave exposure may act in a manner similar to noradrenergic beta-antagonists.
Experiment 2 and 3: Acute low-level microwave exposure attenuated ethanol-induced hypothermia in the rat. The data confirm that ethanol-induced hypothermia is partially mediated by noradrenergic systems. Pretreatment with the centrally active beta-adrenergic antagonist propranolol significantly attenuated the ethanol-induced hypothermia of sham-exposed animals. There was no consistent effect of propranolol on irradiated rats, regardless of dose. Similarly, the degree of hypothermia demonstrated by sham-exposed controls was significantly attenuated compared to exposed rats by pretreatment with the peripheral beta-adrenergic antagonist CGP-12177.
In conclusion, the findings confirm noradrenergic mediation of ethanol-induced hypothermia and suggest that microwave energy may in some way mimic the role of beta-adrenergic antagonists.