Stimulation of the hypothalamic paraventricular nucleus produces analgesia not mediated by vasopressin or endogenous opioids

Raz Yirmiya*, Shamgar Ben-Eliyahu, Yehuda Shavit, Przemyslaw Marek, John C. Liebeskind

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

49 Scopus citations

Abstract

The analgesic effect of electrical stimulation of the hypothalamic paraventricular nucleus (PVN) was studied. Additionally, the involvement of vasopressin and opioid peptides in this process was examined by comparing vasopressin-deficient (Brattleboro) and Long-Evans rats and by administering the opiate antagonist naloxone. Rats were chronically implanted with a stimulating electrode in the parvocellular (PVN-Pc) and magnocellular (PVN-Mg) divisions of the PVN. At least 10 days after surgery, the analgesic effects of PVN stimulation were examined in lightly anesthetized rats, using the tail-flick method, and in unanesthetized rats, using the hot-plate test. PVN stimulation produced marked analgesia in both tests. Current threshold for analgesia was lower from PVN-Pc than from PVN-Mg. Threshold did not differ significantly between Brattleboro and Long-Evans rats and was not affected by naloxone administration. The results indicate that the PVN is part of the brain's pain inhibitory system, and show that the analgesia induced by PVN stimulation is not mediated by either vasopressin or opioid peptides.

Original languageEnglish
Pages (from-to)169-174
Number of pages6
JournalBrain Research
Volume537
Issue number1-2
DOIs
StatePublished - 24 Dec 1990
Externally publishedYes

Keywords

  • Brattleboro
  • Naloxone
  • Opioid
  • Pain
  • Paraventricular nucleus
  • Rat
  • Stimulation-produced analgesia
  • Vasopressin

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