Apamin increases post-spike excitability of supraoptic nucleus neurons in anaesthetized morphine-naïve rats and morphine-dependent rats: consequences for morphine withdrawal excitation

Philip M Bull, John A Russell, Victoria Scott, Colin H Brown

Research output: Contribution to journalArticlepeer-review

Abstract

Supraoptic nucleus (SON) oxytocin neurons develop morphine dependence when chronically exposed to this opiate and undergo excitation when morphine is subsequently withdrawn. Morphine withdrawal excitation is evident as an increased action potential (spike) firing rate and is associated with an increased post-spike excitability that is consistent with the expression of an enhanced post-spike afterdepolarization (ADP) during withdrawal. Here, we administered apamin (which inhibits the medium afterhyperpolarization [mAHP] in vitro and unmasks an ADP) into the SON of urethane-anaesthetized rats to determine its effects on oxytocin neurons in vivo. As predicted, intra-SON apamin administration increased the propensity to fire a spike soon (
Original languageEnglish
Pages (from-to)517-28
Number of pages12
JournalExperimental Brain Research
Volume212
Issue number4
DOIs
Publication statusPublished - Aug 2011

Keywords

  • Animals
  • Morphine
  • Substance Withdrawal Syndrome
  • Morphine Dependence
  • Narcotic Antagonists
  • Apamin
  • Action Potentials
  • Naloxone
  • Oxytocin
  • Rats
  • Rats, Sprague-Dawley
  • Neurons
  • Analgesics, Opioid
  • Female
  • Supraoptic Nucleus

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