Lack of evidence for the μ-opioid receptor splice variant MOR1C in rats

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We previously reported the existence of MOR1C mRNA and MOR1C-immunoreactivity (-ir) in rats. However, the sequence that we reported for rat MOR1C appears not to be present in the rat genome. We have therefore reexamined whether MOR1C mRNA or MOR1C-ir exist in rats. We used reverse-transcription polymerase chain reaction (RT-PCR) to attempt to amplify MOR1, MOR1A, MOR1B, the rat MOR1C sequence we previously reported, and MOR1C1 and MOR1C2 (which have recently been reported to exist in rats). In RNA extracted from rats, we were able to demonstrate PCR products representing MOR1, MOR1A, and MOR1B splice variants. All three products were confirmed as related to MOR1 by Southern blot. However, we were unable to detect either the MOR1C product reported previously by us or the MOR1C-like products reported to exist in rats by others. In RNA extracted from mice we were able to detect MOR1, MOR1A, MOR1B, and MOR1D-like products. To test the specificity of our MOR1C antiserum, we examined MOR1C-ir in control and knockout mice. MOR1C-ir had a distribution in control mice similar to that previously reported in rats, including coexisting with vGLUT2. However, although MOR1-ir was absent in MOR1 knockout mice, the density and distribution of MOR1C-ir were unchanged, suggesting that the antiserum crossreacts with another molecule in tissue. We find no evidence for MOR1C mRNA in rats. Furthermore, we conclude that MOR1C-ir represents crossreactivity.

Original languageEnglish (US)
Pages (from-to)452-458
Number of pages7
JournalJournal of Comparative Neurology
Issue number4
StatePublished - Dec 1 2009


  • Alternative splicing
  • Analgesia
  • Drug abuse
  • Nociception
  • Pain


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