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 complementry to oxytocin-induced hyperactivity and seizures. There data are discussed in terms of tonic versus phasic influences of these peptides upon pain perception.

Human Pain Thresholds after the Application of Lypressin, a Vasopressin Analogue

“…In contrast to the current human study, in animal studies vasopressin has proved effective in suppressing presumably pain-related responses (Berkowitz & Sherman 1982;Berntson & Berson 1980;Berson et a/. 1983;Bodnar et al 1980Bodnar et al & 1984Kordower et al 1982). Species differences may explain this discrepancy.…”

“…There remains the possibility that the application of vasopressin directly to the central nervous system had produced analgesia in our subjects. In some animal studies demonstrating a vasopressin-induced analgesia, intrathecal administration was used (Bodnar et al 1984;Berntson & Berson 1980;Kordower et a/. 1982), although systemic administration has proved effective too (Berson et al 1983;Berntson & Berson 1980).…”

“…Classically vasopressin is also known to have a cardiovascular pressor response. Additionally, recent animal studies have suggested that vasopressin has analgetic properties (Berkowitz & Sherman 1982;Berntson & Berson 1980;Berson et al 1983;Bodnar et al 1980Bodnar et al & 1984Kordower et al 1982). The mechanisms underlying the vasopressin analgesia are still largely unknown.…”

The antinociceptive role of central arginine vasopressin is involved in the endogenous opiate peptide, serotonin and acetylcholine systems

“…However, most of AVP is synthesized in hypothalamic paraventricular nucleus (PVN) and hypothalamic supraoptic nucleus (SON) [2,15]. It has been proven that PVN and SON play an important role in analgesia [16][17][18][19][20], and AVP, which may be from PVN and SON, is involved in pain modulation [21,22]. Our present study showed that (1) not only V 1 recep- Histological study has shown that there are many AVP containing fibers in the periaqueductal gray (PAG), which come from PVN neurons [23,24].…”

Intracerebroventricularly Administered Oxytocin Has No Direct Influence on the Somatosensory System in Anesthetized Rats-Evaluation by Cortical Somatosensory Evoked Potentials.

“…On the contrary, there have been contradictory reports suggesting that the oxytocin-induced analgesia in rodents is an epiphenomenon accompanying a concomitant seizure 3,6) . A direct analgesic role for oxytocin has also been doubted since lesions of the paraventricular nuclei have no effects on nociception 7) .…”