VR1- and VRL-1-like immunoreactivity in normal and injured trigeminal dental primary sensory neurons of the rat

Authors

  • Emma Stenholm Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden; Department of Odontology, Huddinge Hospital, Karolinska Institutet, Huddinge, Sweden
  • Ulf Bongenhielm Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden; Department of Odontology, Huddinge Hospital, Karolinska Institutet, Huddinge, Sweden
  • Michael Ahlquist Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden; Department of Odontology, Huddinge Hospital, Karolinska Institutet, Huddinge, Sweden
  • Kaj Fried Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden; Department of Odontology, Huddinge Hospital, Karolinska Institutet, Huddinge, Sweden

DOI:

https://doi.org/10.1080/000163502753509455

Keywords:

Gingiva, Immunohistochemistry, Tooth, Pulp, Trigeminal, Ganglion, Vr1, Vrl-1, Nerve, Injury

Abstract

The vanilloid receptor VR1 and the vanilloid receptor-like protein VRL-1 are associated with polymodal nociceptors, and may be important for pain processing in normal and injured teeth. Using immunohistochemistry, we have studied the distribution of these receptors in rat pulpal or gingival trigeminal ganglion neurons that were identified through retrograde labeling with fluoro-gold. Twenty-one percent to 34% of tooth pulp-innervating neurons were VR1-positive, while 32%-51% were VRL-1-immunoreactive. However, double-labeling experiments revealed that VR1 and VRL-1 rarely co-existed in the same cells, but rather seemed to be confined to separate subpopulations. Among the gingival neurons, about 25% were VR1-positive and about 41% were VRL-1-immunoreactive. A lesion of the inferior alveolar nerve, which supplies mandibular teeth and gingiva, resulted in a marked down-regulation of VR1 in the affected trigeminal ganglion cells. A down-regulation of VRL-1 was also indicated. The results suggest that both VR1 and VRL-1 could have significant roles in pulpal and gingival nociceptive transduction.

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Published

2002-01-01