Format

Send to

Choose Destination
See comment in PubMed Commons below
Brain Res. 2007 Apr 27;1143:78-82. Epub 2007 Jan 25.

Disruption of acute opioid dependence by antisense oligodeoxynucleotides targeting neurogranin.

Author information

  • 1Department of Biopharmaceutical Sciences and Cancer Center, University of Illinois, Chicago, IL 60612, USA.

Abstract

Neurogranin has been suggested to serve as a common regulator synchronizing the activities of PKC and CaMKII in acute opioid tolerance. To examine if a similar mechanism exists in acute opioid dependence, we directly targeted neurogranin using antisense oligodeoxynucleotides. Male ICR mice were pretreated with neurogranin antisense or mismatch oligodeoxynucleotides (2 microg/day, i.c.v.) for 3 consecutive days. On Day 4, morphine (100 mg/kg, s.c.) was used to induce dependence, as revealed by naloxone-precipitated withdrawal in saline or mismatch-pretreated mice. Antisense-pretreated mice showed decreased neurogranin expression, lack of morphine-induced phosphorylation of neurogranin and activation of CaMKII and CREB, and absence of naloxone-induced withdrawal jumping. Taken together, these data suggest that neurogranin plays an essential role in acute opioid dependence, possibly by affecting the CaMKII and CREB signaling pathway.

PMID:
17306231
DOI:
10.1016/j.brainres.2007.01.058
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center