Selective attenuation of mu-opioid receptor-mediated effects in rat sensory neurons by intrathecal administration of antisense oligodeoxynucleotides
- PMID: 8939470
- DOI: 10.1016/0304-3940(96)13111-6
Selective attenuation of mu-opioid receptor-mediated effects in rat sensory neurons by intrathecal administration of antisense oligodeoxynucleotides
Abstract
To test the hypothesis that the expression of specific proteins on peripheral terminals of primary afferents can be attenuated by intrathecal administration of antisense oligodeoxynucleotides (ODNs), we administered ODNs antisense to the mu-opioid receptor to male Sprague-Dawley rats via chronically implanted intrathecal cannulae. Antisense but not mismatch ODN treatment significantly decreased peripheral (D-Ala2, N-Me-Phe4, Gly5-ol)-enkephalin (DAMGO) inhibition of prostaglandin E2 (PGE2) hyperalgesia. Antisense treatment affected neither the magnitude of PGE2 hyperalgesia nor the antinociception produced by a peripherally administered adenosine A1-agonist. The antinociceptive effects of DAMGO was fully recovered 8 days after cessation of ODN treatment. DAMGO-induced inhibition of voltage-gated Ca2+ currents (VGCC), in cultured dorsal root ganglion (DRG) neurons from rats treated with ODNs, was also significantly reduced by antisense but not mismatch ODNs. Taken together, these observations suggest that intrathecal administration of antisense ODNs can be used to study the function of proteins present in the peripheral terminals of primary afferent neurons.
Similar articles
-
Multiple receptors involved in peripheral alpha 2, mu, and A1 antinociception, tolerance, and withdrawal.J Neurosci. 1997 Jan 15;17(2):735-44. doi: 10.1523/JNEUROSCI.17-02-00735.1997. J Neurosci. 1997. PMID: 8987795 Free PMC article.
-
Selective blockade of peripheral delta opioid agonist induced antinociception by intrathecal administration of delta receptor antisense oligodeoxynucleotide.Neurosci Lett. 1996 Dec 20;220(3):155-8. doi: 10.1016/s0304-3940(96)13262-6. Neurosci Lett. 1996. PMID: 8994216
-
Spinal pretreatment with antisense oligodeoxynucleotides against exon-1, -4, or -8 of mu-opioid receptor clone leads to differential loss of spinal endomorphin-1-and endomorphin-2-induced antinociception in the mouse.J Pharmacol Exp Ther. 2002 Nov;303(2):867-73. doi: 10.1124/jpet.102.038810. J Pharmacol Exp Ther. 2002. PMID: 12388674
-
Loss of TRPV1-expressing sensory neurons reduces spinal mu opioid receptors but paradoxically potentiates opioid analgesia.J Neurophysiol. 2006 May;95(5):3086-96. doi: 10.1152/jn.01343.2005. Epub 2006 Feb 8. J Neurophysiol. 2006. PMID: 16467418
-
Opioid and adenosine peripheral antinociception are subject to tolerance and withdrawal.J Neurosci. 1995 Dec;15(12):8031-8. doi: 10.1523/JNEUROSCI.15-12-08031.1995. J Neurosci. 1995. PMID: 8613740 Free PMC article.
Cited by
-
Role of GPCR (mu-opioid)-receptor tyrosine kinase (epidermal growth factor) crosstalk in opioid-induced hyperalgesic priming (type II).Pain. 2018 May;159(5):864-875. doi: 10.1097/j.pain.0000000000001155. Pain. 2018. PMID: 29447132 Free PMC article.
-
A comparison of the potential role of the tetrodotoxin-insensitive sodium channels, PN3/SNS and NaN/SNS2, in rat models of chronic pain.Proc Natl Acad Sci U S A. 1999 Jul 6;96(14):7640-4. doi: 10.1073/pnas.96.14.7640. Proc Natl Acad Sci U S A. 1999. PMID: 10393873 Free PMC article. Review.
-
Hyperalgesic priming (type II) induced by repeated opioid exposure: maintenance mechanisms.Pain. 2017 Jul;158(7):1204-1216. doi: 10.1097/j.pain.0000000000000898. Pain. 2017. PMID: 28306605 Free PMC article.
-
Multiple neurological abnormalities in mice deficient in the G protein Go.Proc Natl Acad Sci U S A. 1998 Mar 17;95(6):3269-74. doi: 10.1073/pnas.95.6.3269. Proc Natl Acad Sci U S A. 1998. PMID: 9501252 Free PMC article.
-
Role of interleukin-6 in chronic muscle hyperalgesic priming.Neuroscience. 2008 Mar 18;152(2):521-5. doi: 10.1016/j.neuroscience.2008.01.006. Epub 2008 Jan 12. Neuroscience. 2008. PMID: 18280048 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Research Materials
Miscellaneous
