NMDA antagonists and clonidine block c‐fos expression during morphine withdrawal

NMDA antagonists and clonidine block c‐fos expression during morphine withdrawal The c‐fos gene is expressed in the central nervous system (CNS) in response to neuronal stimuli. Induction of c‐fos in certain CNS regions occurs following naltrexone precipitated withdrawal in morphine dependent rats. Non‐competitive (MK801) and competitive (LY274614) NMDA receptor antagonists and clonidine, an alpha2 partial agonist, attenuate the intensity of naltrexone precipitated withdrawal. We determined the levels of c‐fos mRNA by solution hybridization in several brain regions in control and morphine dependent rats following pretreatment with saline, MK801 (1 mg/kg, s.c.), LY274614 (100 mg/kg, i.p.), or clonidine (1.5 mg/kg, i.p.). Morphine treatment increased c‐fos mRNA levels in striatum (STR) and amygdala (AMY). Naltrexone did not alter c‐fos mRNA levels in placebo‐treated rats. However, naltrexone increased c‐fos mRNA levels in morphine dependent rats in the nucleus accumbens (NA), frontal cortex (FC), AMY, and hippocampus (HIP) but not in STR or spinal cord. Pretreatment with MK801 blocked this effect of naltrexone in AMY but not in NA, FC, or HIP, while pretreatment with LY274614 or clonidine blocked this effect of naltrexone in AMY and NA but not in FC or HIP. These results further delineate both the neuroanatomical pathways involved in morphine withdrawal and the locus of action of compounds that reduce morphine‐withdrawal symptoms. © 1995 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Synapse Wiley

NMDA antagonists and clonidine block c‐fos expression during morphine withdrawal

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Publisher
Wiley
Copyright
Copyright © 1995 Wiley‐Liss, Inc.
ISSN
0887-4476
eISSN
1098-2396
DOI
10.1002/syn.890200110
Publisher site
See Article on Publisher Site

Abstract

The c‐fos gene is expressed in the central nervous system (CNS) in response to neuronal stimuli. Induction of c‐fos in certain CNS regions occurs following naltrexone precipitated withdrawal in morphine dependent rats. Non‐competitive (MK801) and competitive (LY274614) NMDA receptor antagonists and clonidine, an alpha2 partial agonist, attenuate the intensity of naltrexone precipitated withdrawal. We determined the levels of c‐fos mRNA by solution hybridization in several brain regions in control and morphine dependent rats following pretreatment with saline, MK801 (1 mg/kg, s.c.), LY274614 (100 mg/kg, i.p.), or clonidine (1.5 mg/kg, i.p.). Morphine treatment increased c‐fos mRNA levels in striatum (STR) and amygdala (AMY). Naltrexone did not alter c‐fos mRNA levels in placebo‐treated rats. However, naltrexone increased c‐fos mRNA levels in morphine dependent rats in the nucleus accumbens (NA), frontal cortex (FC), AMY, and hippocampus (HIP) but not in STR or spinal cord. Pretreatment with MK801 blocked this effect of naltrexone in AMY but not in NA, FC, or HIP, while pretreatment with LY274614 or clonidine blocked this effect of naltrexone in AMY and NA but not in FC or HIP. These results further delineate both the neuroanatomical pathways involved in morphine withdrawal and the locus of action of compounds that reduce morphine‐withdrawal symptoms. © 1995 Wiley‐Liss, Inc.

Journal

SynapseWiley

Published: May 1, 1995

References

  • Development of physical dependance on morphine in respect to time and dosage and quantification of the precipitated withdrawal syndrome in rats
    Blasig, Blasig; Herz, Herz; Reinhold, Reinhold; Zieglgansberger, Zieglgansberger
  • Stimulus‐transcription coupling in the nervous system: Involvement of the inducible proto‐oncogenes fos and jun
    Morgan, Morgan; Curran, Curran
  • Multiple mechanisms of withdrawal from opioid drugs
    Redmond, Redmond; Krystal, Krystal

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