Molecular components of tolerance to opiates in single hippocampal neurons

Mol Pharmacol. 2002 Jan;61(1):55-64. doi: 10.1124/mol.61.1.55.

Abstract

We examined the effect of acute and chronic opioid treatment on synaptic transmission and mu-opioid receptor (MOR) endocytosis in cultures of naïve rat hippocampal neurons. Opioid agonists that activate MOR inhibited synaptic transmission at inhibitory but not excitatory autapses. [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO), morphine, and methadone were all effective at blocking inhibitory transmission. These same drugs also reduced the amplitude of voltage-dependent Ca(2+) currents in inhibitory but not excitatory neurons. Chronic treatment with all three opioids reduced the subsequent effects of a challenge with either the same drug or one of the others in individual autaptic neurons. Chronic treatment with DAMGO or methadone produced internalization of enhanced yellow fluorescent protein-tagged MOR expressed in hippocampal neurons within hours, whereas morphine produced internalization much more slowly, even when accompanied by overexpression of beta-arrestin-2. We conclude that DAMGO, methadone, and morphine all produce tolerance in single hippocampal neurons. Morphine-induced tolerance does not necessarily seem to involve receptor endocytosis.

MeSH terms

  • Animals
  • Arrestins / metabolism
  • Barium / physiology
  • Cells, Cultured
  • Drug Tolerance / physiology*
  • Electrophysiology
  • Hippocampus / cytology
  • Hippocampus / drug effects
  • Narcotics / pharmacology*
  • Neurons / drug effects*
  • Neurons / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, GABA / metabolism
  • Receptors, Opioid, mu / agonists
  • Receptors, Opioid, mu / metabolism
  • Synaptic Transmission / drug effects
  • Tissue Distribution
  • beta-Arrestin 2
  • beta-Arrestins

Substances

  • Arrb2 protein, rat
  • Arrestins
  • Narcotics
  • Receptors, GABA
  • Receptors, Opioid, mu
  • beta-Arrestin 2
  • beta-Arrestins
  • Barium