Dental analgesia produced by non-painful low-frequency stimulation is not influenced by stress or reversed by naloxone.
The dental pain threshold elevation produced by non-painful, low-frequency transcutaneous electrical nerve stimulation (TENS) in healthy humans was not reduced by the administration of 0.8 mg of naloxone i.v. Neither ACTH, prolactin nor growth hormone (GH) release were related to the pain threshold elevations. The present study indicates that the dental pain threshold elevation during non-painful, low-frequency TENS is not based on the same opioid-dependent mechanisms as the dental pain threshold elevation during acupuncture or the clinical analgesia during low-frequency TENS. Stress or other adenohypophyseal mechanisms involving ACTH, prolactin or GH do not explain the analgesia induced by non-painful, low-frequency TENS.
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D003782:Dental Pulp / Q000294:innervation*; D004599:Electric Stimulation Therapy / Q000379:methods*; D004723:Endorphins / Q000502:physiology; D005260:Female; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D009619:Nociceptors / Q000502:physiology*; D011388:Prolactin / Q000097:blood; D012684:Sensory Thresholds; D013312:Stress, Physiological / Q000097:blood*; D001615:beta-Endorphin
D004723:Endorphins; D009270:Naloxone; D001615:beta-Endorphin; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D013006:Growth Hormone