Behavioral and physiological studies of non-narcotic analgesia in the rat elicited by certain environmental stimuli.
These experiments characterized the analgesia resulting from exposure to certain noxious and/or stressful manipulations. Rats exposed either to electric grid shock (0.35-2.0 mA for 10-30 sec) or to 5 min of presumably non-painful centrifugal rotation (about 7.0 transverse g's) were analgesic as measured by tail-flick, hot plate and responses to applications of a calibrated paw pinch or alligator clip. Analgesia produced by shock (SA) or centrifugal rotation (RA) persisted after termination of these manipulations. Neither SA nor RA were attended by generalized sensory, attentional or motoric deficits. Intraperitoneal injection of hypertonic saline also increased tail-flick latencies. Exposure to brief ether anesthesia or horizontal oscillation, both of which have been reported to increase ACTH secretion (a commonly used indicator of stress), did not produce analgesia as measured by the tail-flick test. The use of classical conditioning procedures to pair shock with environmental stimuli resulted in increased tail-flick latencies. The narcotic antagonist naloxone (1 mg/kg, i.p.) did not reduce the tail-flick inhibition produced by shock, rotation, hypertonic saline or classical conditioning. Chlordiazepoxide (5 mg/kg, i.p.) also failed to antagonize the increased tail-flick latencies produced by shock or conditioning. Tail-flick inhibition produced by shock or rotation was markedly reduced by complete spinal cord transection at thoracic levels. These results suggest that: (1) the selective modulation of nociceptive input at the level of the spinal cord can be mediated by a supraspinal system or systems physiologically distinct from those involved in analgesia produced by the administration of opiates; (2) non-narcotic modulation of nociceptive input occurring within the spinal cord can be learned by exposure to classical conditioning procedures; and (3) noxious stimuli are sufficient but not necessary to produce a non-narcotic analgesia; stress alone, however, is not always sufficient to produce this analgesia.
D000698:Analgesia; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology*; D002707:Chlordiazepoxide / Q000494:pharmacology; D003214:Conditioning, Classical / Q000502:physiology; D004597:Electroshock; D004987:Ethers / Q000494:pharmacology; D005260:Female; D007274:Injections, Intraperitoneal; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology*; D011292:Premedication; D051381:Rats; D012018:Reflex / Q000502:physiology; D012399:Rotation; D012462:Saline Solution, Hypertonic; D012684:Sensory Thresholds / Q000187:drug effects; D013116:Spinal Cord / Q000502:physiology
D004987:Ethers; D012462:Saline Solution, Hypertonic; D009270:Naloxone; D002707:Chlordiazepoxide