Thermal analgesia induced by 30-min exposure to 1 microT burst-firing magnetic fields is strongly enhanced in a dose-dependent manner by the alpha2 agonist clonidine in rats.
Most of the research concerning analgesia following brief exposures to physiologically patterned weak magnetic fields has focused upon their morphine-related properties. However, the alpha-adrenergic system interacts with morphine-induced analgesia. In the present study we found that prazosin, phenylephrine, and yohimbine did not augment the robust analgesia to thermal stimuli in rats evoked by whole-body exposures to a 1 microT, burst-firing magnetic field presented once every 4s for 30 min. However, the alpha2 agonist clonidine enhanced the field-induced analgesia in a dose-dependent manner that reflected a receptor-saturation response. Potentiation between the field and clonidine was evident at 0.2 mg/kg and approached asymptote at 1 mg/kg. The combination of the effects from exposure to the magnetic field and the clonidine explained more than 75% of the variance in the change in nociceptive thresholds from baseline levels. The possibility that properly patterned weak magnetic fields could be a powerful adjunct to pharmacological treatments of pain is considered.
Behavioral Neuroscience Laboratory, Department of Biology, Laurentian University, Sudbury, Ont., P3E 2C6, Canada.
L J
LJ
Martin
M A
MA
Persinger
D058647:Adrenergic alpha-2 Receptor Agonists; D000698:Analgesia / Q000379:methods*; D000818:Animals; D003000:Clonidine / Q000494:pharmacology*; D004574:Electromagnetic Fields; D006361:Heating; D008280:Magnetics; D008297:Male; D010147:Pain Measurement; D051381:Rats; D017208:Rats, Wistar; D014916:Whole-Body Irradiation
D058647:Adrenergic alpha-2 Receptor Agonists; D003000:Clonidine