Morphine causes a delayed increase in glutamate receptor functioning in the nucleus accumbens core

Eur J Pharmacol. 2005 Mar 21;511(1):27-30. doi: 10.1016/j.ejphar.2005.02.009.

Abstract

Enhanced excitatory neurotransmission in the mesocorticolimbic system may contribute to the persistence of addiction behaviour. Here, we demonstrated that glutamate-, N-methyl-D-aspartate (NMDA)- and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)-induced [3H]-gamma-aminobutyric acid (GABA) release from superfused rat nucleus accumbens core slices is profoundly enhanced 3 weeks, but not 3 days, after a single s.c. morphine injection. This delayed increase in glutamate receptor functioning is associated with enhanced gene transcript levels of ionotropic NMDA and AMPA/kainate receptor subunits. These data reveal that morphine may progressively enhance glutamate neurotransmission within the nucleus accumbens core subsequent to drug exposure.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Glutamic Acid / pharmacology
  • Injections, Subcutaneous
  • Male
  • Morphine / administration & dosage
  • Morphine / pharmacology*
  • N-Methylaspartate / pharmacology
  • Nucleus Accumbens / drug effects*
  • Nucleus Accumbens / metabolism
  • Potassium / pharmacology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Receptors, Glutamate / genetics
  • Receptors, Glutamate / physiology*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Time Factors
  • Transcription, Genetic / drug effects
  • Tritium
  • alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / pharmacology
  • gamma-Aminobutyric Acid / metabolism

Substances

  • RNA, Messenger
  • Receptors, Glutamate
  • Tritium
  • Glutamic Acid
  • gamma-Aminobutyric Acid
  • N-Methylaspartate
  • Morphine
  • alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
  • Potassium