Disruption of acute opioid dependence by antisense oligodeoxynucleotides targeting neurogranin

Lei Tang, Pradeep Kumar Shukla, Zaijie Jim Wang

Research output: Contribution to journalArticle

8 Citations (Scopus)

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 μg/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.

Original languageEnglish (US)
Pages (from-to)78-82
Number of pages5
JournalBrain Research
Volume1143
Issue number1
DOIs
StatePublished - Apr 27 2007
Externally publishedYes

Fingerprint

Neurogranin
Oligodeoxyribonucleotides
Opioid Analgesics
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Naloxone
Morphine
Inbred ICR Mouse
Phosphorylation

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Developmental Biology
  • Clinical Neurology

Cite this

Disruption of acute opioid dependence by antisense oligodeoxynucleotides targeting neurogranin. / Tang, Lei; Shukla, Pradeep Kumar; Wang, Zaijie Jim.

In: Brain Research, Vol. 1143, No. 1, 27.04.2007, p. 78-82.

Research output: Contribution to journalArticle

@article{49e6dd6f449a440ab7907d8c7bb79d0a,
title = "Disruption of acute opioid dependence by antisense oligodeoxynucleotides targeting neurogranin",
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 μg/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.",
author = "Lei Tang and Shukla, {Pradeep Kumar} and Wang, {Zaijie Jim}",
year = "2007",
month = "4",
day = "27",
doi = "10.1016/j.brainres.2007.01.058",
language = "English (US)",
volume = "1143",
pages = "78--82",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Disruption of acute opioid dependence by antisense oligodeoxynucleotides targeting neurogranin

AU - Tang, Lei

AU - Shukla, Pradeep Kumar

AU - Wang, Zaijie Jim

PY - 2007/4/27

Y1 - 2007/4/27

N2 - 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 μg/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.

AB - 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 μg/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.

UR - http://www.scopus.com/inward/record.url?scp=33947303389&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33947303389&partnerID=8YFLogxK

U2 - 10.1016/j.brainres.2007.01.058

DO - 10.1016/j.brainres.2007.01.058

M3 - Article

VL - 1143

SP - 78

EP - 82

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -