Background
Tumor necrosis factor-α (TNF-α) is emerging as an important modulator of the function
of the central nervous system (CNS). We have demonstrated that TNF-α or Leu-Ile, a
TNF-α inducer, inhibits methamphetamine-induced rewarding effects and sensitization.
In this study, we investigated the effects of TNF-α or Leu-Ile on morphine (MOR)-induced
rewarding effects and sensitization.
Methods
Levels of TNF-α messenger RNA (mRNA) and protein were determined by real-time reverse
transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. Effects
of TNF-α or Leu-Ile on MOR-induced rewarding effects and sensitization were investigated
by conditioned place preference and locomotor activity tests. Extracellular dopamine
levels were examined using in vivo microdialysis. Effects of TNF-α or Leu-Ile on MOR-induced
antinociceptive effect and withdrawal symptoms were examined by hot plate test and
naloxone-preciptated withdrawal.
Results
Morphine induced TNF-α mRNA expression via dopamine and opioid receptors. Posttreatment
with TNF-α or Leu-Ile attenuated the MOR-induced place preference and sensitization
even after their development, as well as pretreatment with TNF-α or Leu-Ile blocked
them. An inhibitory effect of Leu-Ile on MOR-induced place preference was not observed
in TNF-α knockout mice. Tumor necrosis factor-α or Leu-Ile inhibited the increase
in extracellular dopamine levels in the nucleus accumbens induced by repeated MOR
treatment.
Conclusions
These results suggest that TNF-α inhibits MOR-induced rewarding effect and sensitization
by regulating extracellular dopamine levels, and Leu-Ile inhibits them via the induction
of TNF-α.
Key Words
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Article info
Publication history
Published online: January 11, 2007
Accepted:
October 4,
2006
Received in revised form:
September 30,
2006
Received:
May 23,
2006
Identification
Copyright
© 2007 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
