Pain Threshold Changes in Rats Following Central Injection of Beta-Endorphin, Met-Enkephalin, Vasopressin or Oxytocin Antisera

Abstract

Both opioid peptides such as beta-endorphin and met-enkephalin and nonopioid peptides such as vasopressin and oxytocin increase pain thresholds in rodents. Antisera raised against each of these peptides have been developed for use in immunocytochemical and radioimmunoassay procedures. The present study assessed whether central administration of antisera raised against beta-endorphin (ABE), met-enkephalin (AME), arginine vasopressin (AAVP) or oxytocin (AOT) altered tail-flick latencies elicited by three different levels of radiant heat, jump thresholds, core body temperatures and locomotor activity. ABE induced a transient hyperalgesia on the tail-flick test at thermal levels at which beta-endorphin administration would elicit an analgesic effect. While met-enkephalin increases tail-flick latencies elicited by high thermal levels, AME failed to alter latencies at this level, but rather induced a short-acting hyperalgesia at a low thermal level. While vasopressin increased tail-flick latencies at high thermal levels, AAVP produced reciprocal decreases. Yet AAVP inexplicably induced analgesic effects at moderate and low thermal levels. Finally, while oxytocin increased latencies at high thermal levels, AOT failed to alter latencies. Rather, it decreased latencies at the moderate thermal level and increased latencies at the low thermal level. Neither jump thresholds nor core body temperatures were affected by any antiserum pretreatment. While activity levels were unaffected by either ABE, AME or AAVP pretreatment, AOT decreased activity in a fashion complements to oxytocin-induced hyperactivity and seizures. There data are discussed in terms of tonic versus phasic influences of these peptides upon pain perception.